You seem to have javascript disabled. Please note that many of the page functionalities won't work as expected without javascript enabled.

Search for Articles:

Title / Keyword

Author / Affiliation / Email

Journal

Article Type

Advanced Search

Section

Special Issue

Volume

Issue

Number

Page

Logical OperatorOperator

Search Text

Search Type

Metabolic Regulation of Ferroptosis in Breast Cancer
Reactive Oxygen Species Across Death Pathways: Gatekeepers of Apoptosis, Ferroptosis, Pyroptosis, Paraptosis, and Beyond
Fusobacterium Nucleatum in Colorectal Cancer: Relationship Among Immune Modulation, Potential Biomarkers and Therapeutic Implications
Chronic Stress and Autoimmunity: The Role of HPA Axis and Cortisol Dysregulation
Astatine-211-Labeled Therapy Targeting Amino Acid Transporters: Overcoming Drug Resistance in Non-Small Cell Lung Cancer

Journal Description

International Journal of Molecular Sciences

International Journal of Molecular Sciences is an international, peer-reviewed, open access journal providing an advanced forum for biochemistry, molecular and cell biology, molecular biophysics, molecular medicine, and all aspects of molecular research in chemistry, and published semimonthly online by MDPI. The Epigenetics Society, European Chitin Society (EUCHIS), Spanish Society for Cell Biology (SEBC) and others are affiliated with IJMS and their members receive a discount on the article processing charges.

Open Access— free for readers, with article processing charges (APC) paid by authors or their institutions.
High Visibility: indexed within Scopus, SCIE (Web of Science), PubMed, PMC, MEDLINE, Embase, CAPlus / SciFinder, and other databases.
Journal Rank: JCR - Q1 (Biochemistry and Molecular Biology) / CiteScore - Q1 (Organic Chemistry)
Rapid Publication: manuscripts are peer-reviewed and a first decision is provided to authors approximately 17.8 days after submission; acceptance to publication is undertaken in 2.6 days (median values for papers published in this journal in the second half of 2025).
Recognition of Reviewers: reviewers who provide timely, thorough peer-review reports receive vouchers entitling them to a discount on the APC of their next publication in any MDPI journal, in appreciation of the work done.
Testimonials: See what our editors and authors say about IJMS.
Companion journals for IJMS include: Biophysica, Stresses, Lymphatics and SynBio.

Impact Factor: 4.9 (2024); 5-Year Impact Factor: 5.7 (2024)

Imprint Information Journal Flyer Open Access ISSN: 1422-0067

Latest Articles

30 pages, 9581 KB

Open AccessArticle

Maternal Nutrient Restriction Programs Fetal Hepatic DNA Methylation in Ovine Monozygotic Twins

by Megan E. Miller, Emilie C. Baker and Michael C. Satterfield

Int. J. Mol. Sci. 2026, 27(3), 1553; https://doi.org/10.3390/ijms27031553 - 4 Feb 2026

Maternal nutrient restriction (MNR) heightens disease susceptibility in offspring through epigenetic modifications that alter the development of essential organs. This study investigates how restriction alters the fetal sheep hepatic methylome and its potential regulatory influence on gene expression. Using a monozygotic twin model [...] Read more.

Maternal nutrient restriction (MNR) heightens disease susceptibility in offspring through epigenetic modifications that alter the development of essential organs. This study investigates how restriction alters the fetal sheep hepatic methylome and its potential regulatory influence on gene expression. Using a monozygotic twin model generated through embryo splitting, we examined hepatic DNA methylation responses to maternal nutrient restriction (50% vs. 100% NRC nutritional requirements; n = 4 per group) from gestational day (GD) 35 to 135 in pregnant sheep. At GD 135, conceptus (fetal–placental unit) development was assessed; although fetal weight was unaffected (p > 0.10), restricted fetuses exhibited reduced liver mass (p < 0.05). Whole-genome bisulfite sequencing (WGBS) of fetal liver identified 1,636,305 differentially methylated CpG sites (dmCpGs) in the Group-Level Analyses and 42,231 dmCpGs in the Twin-Pair Analyses. At the Group-Level, 40,533 promoter, 126,667 exonic, and 785,381 intronic sites were identified, whereas the Twin-Pair subset contained 1314, 7116, and 22,239, respectively. Site-level shifts and functional enrichment across features highlighted GPCR–cAMP/calcium–PI3K/AKT signaling, phosphoinositide metabolism, ECM/integrin–focal adhesion networks, thyroid hormone signaling, and Rho-family GTPases. These findings indicate that maternal nutrient restriction modifies the fetal hepatic methylome through coordinated signaling, metabolic, and structural reconfigurations that create conditions conducive to metabolic disease. Full article

(This article belongs to the Section Molecular Biology)

23 pages, 4862 KB

Open AccessReview

The Roles of Topoisomerases in Transcriptional Regulation

by Kelli D. Fenelon and Ram Madabhushi

Int. J. Mol. Sci. 2026, 27(3), 1552; https://doi.org/10.3390/ijms27031552 - 4 Feb 2026

Torsional stress from DNA supercoiling is receiving renewed attention as a driving force for chromosome folding and the establishment of gene activity states. Transcription is a major source of DNA supercoiling, while topoisomerases relax supercoils and solve topological problems that arise during DNA [...] Read more.

Torsional stress from DNA supercoiling is receiving renewed attention as a driving force for chromosome folding and the establishment of gene activity states. Transcription is a major source of DNA supercoiling, while topoisomerases relax supercoils and solve topological problems that arise during DNA replication, transcription, and chromosome segregation. Recent technological advancements have allowed for the mapping of how torsional stress distributes within the genome and distinguishing between occupancy of topoisomerases on chromatin and sites where they are catalytically engaged. Coupling these innovations to assessments of 3D chromosome conformation and nascent transcription at high resolution have provided a new understanding of the relationships between supercoiling and topoisomerase activity. Here, we summarize the insights obtained from these recent studies and discuss how the interplay between transcription, supercoiling, and topoisomerases shapes cellular gene activity states. Full article

(This article belongs to the Special Issue DNA, Chromatin and Genome Structure)

► Show Figures

Figure 1

14 pages, 1787 KB

Open AccessArticle

Multi-Omics Analysis of Morbid Obesity Using a Patented Unsupervised Machine Learning Platform: Genomic, Biochemical, and Glycan Insights

by Irena Šnajdar, Luka Bulić, Andrea Skelin, Leo Mršić, Mateo Sokač, Maja Brkljačić, Martina Matovinović, Martina Linarić, Jelena Kovačić, Petar Brlek, Gordan Lauc, Martina Smolić and Dragan Primorac

Int. J. Mol. Sci. 2026, 27(3), 1551; https://doi.org/10.3390/ijms27031551 - 4 Feb 2026

Morbid obesity is a complex, multifactorial disorder characterized by metabolic and inflammatory dysregulation. The aim of this study was to observe changes in obese patients adhering to a personalized nutrition plan based on multi-omic data. This study included 14 adult patients with a [...] Read more.

Morbid obesity is a complex, multifactorial disorder characterized by metabolic and inflammatory dysregulation. The aim of this study was to observe changes in obese patients adhering to a personalized nutrition plan based on multi-omic data. This study included 14 adult patients with a body mass index (BMI) > 40 kg/m² who were consecutively recruited from those presenting to our outpatient clinic and who met the inclusion criteria. Clinical, biochemical, hormonal, and glycomic parameters were assessed, along with whole-genome sequencing (WGS) that included a focused analysis of obesity-associated genes and an extended analysis encompassing genes related to cardiometabolic disorders, hereditary cancer risk, and nutrigenetic profiles. Patients were stratified into nutrigenetic clusters using a patented unsupervised machine learning platform (German Patent Office, No. DE 20 2025 101 197 U1), which was employed to generate personalized nutrigenetic dietary recommendations for patients with morbid obesity to follow over a six-month period. At baseline, participants exhibited elevated glucose, insulin, homeostatic model assessment for insulin resistance (HOMA-IR), triglycerides, and C-reactive protein (CRP) levels, consistent with insulin resistance and chronic low-grade inflammation. The majority of participants harbored risk alleles within the fat mass and obesity-associated gene (FTO) and the interleukin-6 gene (IL-6), together with multiple additional significant variants identified across more than 40 genes implicated in metabolic regulation and nutritional status. Using an AI-driven clustering model, these genetic polymorphisms delineated a uniform cluster of patients with morbid obesity. The mean GlycanAge index (56 ± 12.45 years) substantially exceeded chronological age (32 ± 9.62 years), indicating accelerated biological aging. Following a six-month personalized nutrigenetic dietary intervention, significant reductions were observed in both BMI (from 52.09 ± 7.41 to 34.6 ± 9.06 kg/m², p < 0.01) and GlycanAge index (from 56 ± 12.45 to 48 ± 14.83 years, p < 0.01). Morbid obesity is characterized by a pro-inflammatory and metabolically adverse molecular signature reflected in accelerated glycomic aging. Personalized nutrigenetic dietary interventions, derived from AI-driven analysis of whole-genome sequencing (WGS) data, effectively reduced both BMI and biological age markers, supporting integrative multi-omics and machine learning approaches as promising tools in precision-based obesity management. Full article

(This article belongs to the Special Issue Molecular Studies on Obesity and Related Diseases)

► Show Figures

Figure 1

15 pages, 2205 KB

Open AccessArticle

Activation of the S100A8/A9 Alarmin Amplifies Inflammatory Pathways in Equine Ascending Placentitis

by Kirsten E. Scoggin, Shimaa I. Rakha, Ahmed M. Abdellatif, Fatma Adlan, Yosra A. Helmy, Rebecca Ruby, Barry Ball, Yatta Boakari and Hossam El-Sheikh Ali

Int. J. Mol. Sci. 2026, 27(3), 1550; https://doi.org/10.3390/ijms27031550 - 4 Feb 2026

Ascending placentitis is a significant cause of equine pregnancy loss, yet the upstream inflammatory triggers are poorly defined. Recently, we identified S100A8/S100A9 (S100A8/A9) alarmins as potential upstream regulators in a chronic equine placentitis model. The current study aimed to determine whether this upregulation [...] Read more.

Ascending placentitis is a significant cause of equine pregnancy loss, yet the upstream inflammatory triggers are poorly defined. Recently, we identified S100A8/S100A9 (S100A8/A9) alarmins as potential upstream regulators in a chronic equine placentitis model. The current study aimed to determine whether this upregulation is sustained in the acute model and in clinical cases, and to elucidate the expression of their downstream inflammatory mediators. Using an experimental model, we quantified S100A8/A9 mRNA expression in acute (n = 5) and chronic (n = 6) placentitis induced by Streptococcus equi ssp. zooepidemicus. We found mRNA expression of S100A8 and S100A9 was significantly upregulated in chorioallantois during both acute (p < 0.001) and chronic (p < 0.0001) disease compared to controls (n = 5), demonstrating their role is not limited to chronic pathology. A strong positive correlation (r = 0.945) underscored their coordinated expression. Immunohistochemistry revealed minimal staining in controls but dense infiltrations of S100A8/A9-positive neutrophils and macrophages in placentitis tissues. To define the clinical relevance of the downstream pathway, we analyzed RNA sequencing data from clinical placentitis cases (placentitis, n = 4) compared to normal postpartum placenta (control, n = 4). This confirmed upregulation of S100A8/A9 and revealed a concurrent increase in their receptors (TLR4, RAGE) and a spectrum of NF-κB-driven effectors, including pro-inflammatory cytokines (IL1β, IL6, TNF), chemokines (CXCL8, CCL2, CXCL10), and the apoptotic mediator CASP3. Our findings establish that S100A8/A9 upregulation is a sustained feature of equine placentitis and delineates a coherent S100A8/A9-TLR4/RAGE-NF-κB signaling axis that drives inflammation and tissue damage in clinical disease. These findings highlight the diagnostic potential of S100A8/A9 and position this alarmin system as a promising therapeutic target for mitigating infection-induced pregnancy loss. Full article

(This article belongs to the Special Issue Molecular Insights into Placental Pathology)

16 pages, 7233 KB

Open AccessArticle

Berberine Ameliorates DSS-Induced Colitis via Regulation of Mucosal Barrier Homeostasis and Mucin-Degrading Microbiota

by Yanli Chen, Yan Wang, Yanmin He, Lei Qiao, Weilong Dai, Yalin Liu, Xiaoxi Lu, Yujie Gan, Lu Sun, Mingzhi Yang, Yizhen Wang, Jie Fu and Mingliang Jin

Int. J. Mol. Sci. 2026, 27(3), 1549; https://doi.org/10.3390/ijms27031549 - 4 Feb 2026

Berberine, a benzyl isoquinoline alkaloid, is used in food for its diverse spectrum of biological activities. Inflammatory bowel disease (IBD) is a widespread condition characterized by frequent occurrence and limited therapeutic success. Berberine has been shown to alleviate colitis through enhancement of the [...] Read more.

Berberine, a benzyl isoquinoline alkaloid, is used in food for its diverse spectrum of biological activities. Inflammatory bowel disease (IBD) is a widespread condition characterized by frequent occurrence and limited therapeutic success. Berberine has been shown to alleviate colitis through enhancement of the intestinal barrier and modulation of gut microbial balance. However, the further mutualistic balance mechanism between microbes and the mucus of berberine in alleviating IBD still needs to be clarified. Our findings demonstrated a strong association between berberine’s therapeutic efficacy and alterations in the gut microbiota. This includes enhancements in the level of IgA-coated bacteria, Zg16, Reg3g, and Pla2g2a, all of which contribute to microbiota homeostasis. Moreover, the beneficial effect on gut barrier function of berberine was mostly attributed to Akkermansiam and Bacteriodes-associated mucin–SCFA metabolism. This study lays a critical groundwork for the development of berberine-based functional food additives that harness its nutraceutical potential. Full article

(This article belongs to the Special Issue Molecular Research in Animal Nutrition)

► Show Figures

Graphical abstract

29 pages, 8944 KB

Open AccessReview

Metal–Organic Framework-Based Drug Delivery Systems for Cancer Therapy: A Review

by Sedigheh Hatami, Khaled Chahrour, Joelle El Fakhouri, Fares Mohammed, Rana Sabouni and Ghaleb A. Husseini

Int. J. Mol. Sci. 2026, 27(3), 1548; https://doi.org/10.3390/ijms27031548 - 4 Feb 2026

Cancer remains one of the most significant global health challenges, with conventional treatments limited by side effects and resistance to drugs. The unique properties of metal–organic frameworks (MOFs), which offer high surface areas, tunable structures, and biodegradable properties, make them promising candidates for [...] Read more.

Cancer remains one of the most significant global health challenges, with conventional treatments limited by side effects and resistance to drugs. The unique properties of metal–organic frameworks (MOFs), which offer high surface areas, tunable structures, and biodegradable properties, make them promising candidates for cancer therapy. This review focuses on MOF-based drug delivery systems for cancer treatment in biomedical applications. This article discusses various synthesis methods, drug-loading strategies, and cytotoxicity considerations. The relationship between the basic chemistry of MOFs and their biomedical applications is elucidated by how each feature directly affects MOF performance in cancer drug delivery. Therefore, this review is a practical and complete guide for researchers working to translate MOFs into effective cancer treatments. Moreover, the role of stimuli-responsive MOFs in cancer therapy is highlighted, along with recent studies demonstrating the effectiveness of MOF-based drug delivery systems. Overall, MOFs offer opportunities for advancing cancer treatment and controlled drug delivery. Full article

(This article belongs to the Section Molecular Oncology)

20 pages, 1827 KB

Open AccessArticle

Nephroprotective Effect of Methanolic Extract of Micromeria frivaldszkyana (Degen) Velen Against Acetaminophen Overdose in Rats

by Elisaveta Apostolova, Vesela Kokova, Ivica Dimov, Mariya Choneva, Delyan Delev, Ilia Kostadinov, Ilia Bivolarski, Maria Koleva, Tsvetelina Mladenova, Krasimir Todorov and Anelia Bivolarska

Int. J. Mol. Sci. 2026, 27(3), 1547; https://doi.org/10.3390/ijms27031547 - 4 Feb 2026

Acetaminophen (APAP) overdose can induce potentially fatal nephrotoxicity. Micromeria frivaldszkyana (M. frivaldszkyana), an endemic plant to Bulgaria, has demonstrated significant antioxidant activity. This study represents the first evaluation of the nephroprotective effects of a methanolic extract of M. frivaldszkyana in an APAP-induced rat [...] Read more.

Acetaminophen (APAP) overdose can induce potentially fatal nephrotoxicity. Micromeria frivaldszkyana (M. frivaldszkyana), an endemic plant to Bulgaria, has demonstrated significant antioxidant activity. This study represents the first evaluation of the nephroprotective effects of a methanolic extract of M. frivaldszkyana in an APAP-induced rat model of kidney injury. The aim of the study was to investigate the protective potential of orally administered M. frivaldszkyana methanolic extract against APAP-induced nephrotoxicity. Male Wistar rats received a one-week treatment with saline, M. frivaldszkyana extract (250, 400, or 500 mg/kg), rosmarinic acid (100 mg/kg), or silymarin (125 mg/kg). On day 7, renal injury was induced by oral administration of APAP (2000 mg/kg). Forty-eight hours later, blood and kidney samples were collected for biochemical and histological analyses. The extract at 500 mg/kg significantly reduced the elevated levels of serum urea (1.83 ± 0.24 vs. 3.49 ± 0.75, p < 0.05), creatinine (59.51 ± 2.30 vs. 72.27 ± 3.92, p < 0.05), and uric acid (477.55 ± 52.48 vs. 898.33 ± 65.30, p < 0.001), while restoring renal glutathione (GSH) levels (4.43 ± 0.19 vs. 2.64 ± 0.10, p < 0.001) and catalase activity (3802.78 ± 142.05 vs. 2485.03 ± 143.23, p < 0.01), compared with APAP-treated rats. Malondialdehyde levels were significantly reduced by the extract (25.19 ± 0.95 vs. 69.66 ± 4.11, p < 0.001), with similar effects observed across all tested doses. In conclusion, M. frivaldszkyana methanolic extract confers significant protection against APAP-induced nephrotoxicity, likely through antioxidant-mediated mechanisms, enhanced GSH restoration, and attenuation of lipid peroxidation, highlighting its potential as a nephroprotective agent. Full article

(This article belongs to the Special Issue Plant Natural Products for Human Health and Disease)

► Show Figures

Figure 1

19 pages, 2374 KB

Open AccessArticle

Preimplantation Genetic Testing of Spinocerebellar Ataxia Type 2—Robust Tools for Direct and Indirect Detection of the ATXN2 CAG Repeat Expansion

by Nur Asherah, Mulias Lian, Arnold S. Tan, Riho Taguchi, Pengyian Chua, Shuling Liu, Caroline G. Lee and Samuel S. Chong

Int. J. Mol. Sci. 2026, 27(3), 1546; https://doi.org/10.3390/ijms27031546 - 4 Feb 2026

Spinocerebellar ataxia type 2 (SCA2) is an autosomal dominant neurodegenerative disorder caused by a pathogenic CAG trinucleotide repeat expansion in the ATXN2 gene. At-risk couples can embark on unaffected pregnancies through preimplantation genetic testing of monogenic disorders (PGT-M) of SCA2, which should involve [...] Read more.

Spinocerebellar ataxia type 2 (SCA2) is an autosomal dominant neurodegenerative disorder caused by a pathogenic CAG trinucleotide repeat expansion in the ATXN2 gene. At-risk couples can embark on unaffected pregnancies through preimplantation genetic testing of monogenic disorders (PGT-M) of SCA2, which should involve accurate repeat expansion detection together with risk haplotype tracking using informative linked markers. Two couples underwent SCA2 PGT-M involving analysis of whole genome amplified embryonic trophectoderm cells by ATXN2 (CAG)n triplet-primed PCR (TP-PCR) and linkage-based risk allele genotyping using customized markers. To simplify and expedite the identification of informative markers for future PGT-M cases, putative microsatellite markers closely linked to ATXN2 were initially screened for polymorphism using a small set of anonymous DNA samples obtained from Coriell Cell Repository. Shortlisted markers with high polymorphism likelihood were then multiplexed in a single-tube reaction and genotyped on 190 anonymous DNA samples to determine their polymorphic information content. Across both SCA2 PGT-M clinical cases, the linked marker genotypes corroborated the TP-PCR results, allowing clear differentiation between unaffected and affected embryos. In both cases, transfer of an unaffected embryo led to a successful pregnancy and live birth of a healthy baby. In silico mining, filtering, and curation identified 287 microsatellites located within 1.65 Mb of either side of the ATXN2 CAG repeat. Of these, eight upstream and nine downstream polymorphic markers were successfully co-amplified in a single-tube assay and demonstrated high overall heterozygosity in both Chinese and Caucasian populations. Conclusion: To ensure high diagnostic accuracy for PGT-M of SCA2, we developed a heptadecaplex microsatellite marker panel for haplotype-based linkage analysis to complement TP-PCR-based direct detection of the ATXN2 CAG repeat. The panel can rapidly identify informative markers from virtually any couple, and it works equally well on MDA-amplified DNAs for embryonic haplotype analysis. Full article

(This article belongs to the Special Issue Preimplantation Genetic Testing in Assisted Reproductive Technologies)

25 pages, 2126 KB

Open AccessReview

The Role of Probiotics Limosilactobacillus reuteri, Ligilactobacillus salivarius, and Lactobacillus johnsonii in Inhibziting Pathogens, Maintaining Gut Health, and Improving Disease Outcomes

by Li Li, Xiangqi Qiu, Shengyong Lu, Haitao Yu, Panpan Lu, Sumei Zeng, Aihua Deng, Min Zhu, E Xu and Jin Niu

Int. J. Mol. Sci. 2026, 27(3), 1545; https://doi.org/10.3390/ijms27031545 - 4 Feb 2026

As the critical component of the gastrointestinal tract, which lives in trillions of gut microorganisms, in a healthy state, the host interacts with the gut microbiota and is symbiotic. The species Limosilactobacillus reuteri, Ligilactobacillus salivarius, and Lactobacillus johnsonii are indigenous gut [...] Read more.

As the critical component of the gastrointestinal tract, which lives in trillions of gut microorganisms, in a healthy state, the host interacts with the gut microbiota and is symbiotic. The species Limosilactobacillus reuteri, Ligilactobacillus salivarius, and Lactobacillus johnsonii are indigenous gut commensal bacteria that are mainly found in the digestive tracts. These three bacteria possess a variety of characteristics that reflect their ability to adapt to the gastrointestinal environment. Herein, we summarize the current progress of research on the probiotic properties of these strains in terms of their ability to protect against harmful pathogens, maintain intestinal health, and improve disease outcomes. These bacteria can impact the intestinal barrier function and enhance intestinal immunity through various mechanisms, such as upregulating the tight-junction protein expression and mucin secretion of intestinal epithelial cells, adjusting and balancing the gut microbiota, and blocking pro-inflammatory cytokine production. They have been shown to ameliorate intestinal inflammation in animal models and provide protective effects against various healthy issues in humans, including diarrhea, constipation, colorectal cancer, obesity, and liver diseases. However, the detailed mechanisms of certain strains remain unclear. Full article

(This article belongs to the Special Issue The Gut Microbiota—Its Role and Molecular Mechanisms in Nutritional Health)

► Show Figures

Figure 1

18 pages, 2575 KB

Open AccessArticle

Uncovering a Glaucoma-Linked Lysophosphatidic Acid–MAPK/AP-1 Fibrosis Axis in Human Trabecular Meshwork Cells and Its Modulation by Diospyros kaki Leaf Extract

by Youngsic Jeon, Hyukjoon Kwon, Hong Ryul Ahn, Gyuwon Huh, Taejung Kim, Young-Tae Park, Hyun Bong Park, Jin-hyoung Jeong, Jae-hyun Jo, Young-Joo Kim and Sang Hoon Jung

Int. J. Mol. Sci. 2026, 27(3), 1544; https://doi.org/10.3390/ijms27031544 - 4 Feb 2026

Dysregulated extracellular matrix (ECM) deposition and epithelial–mesenchymal transition (EMT) in the trabecular meshwork (TM) contribute to glaucoma-associated fibrotic remodeling, and lysophosphatidic acid (LPA) potently induces these profibrotic responses in human trabecular meshwork (HTM) cells. We investigated whether an ethanolic extract of Diospyros kaki [...] Read more.

Dysregulated extracellular matrix (ECM) deposition and epithelial–mesenchymal transition (EMT) in the trabecular meshwork (TM) contribute to glaucoma-associated fibrotic remodeling, and lysophosphatidic acid (LPA) potently induces these profibrotic responses in human trabecular meshwork (HTM) cells. We investigated whether an ethanolic extract of Diospyros kaki leaves (EEDK) attenuates LPA-induced fibrosis and explored the underlying mechanisms. HTM cells were stimulated with LPA and treated with ethanol-based EEDK extracts. Expression of ECM/fibrosis-related genes (FN1, ACTA2, COL1A1, COL3A1, COL4A1, COL6A2, CCN2) and EMT markers (CDH2, VIM, SNAI1) was assessed, along with cell migration using a wound-healing assay. Upstream regulatory pathways were examined via transcription factor prediction, AP-1 reporter assays, and analyses of MAPK/AP-1 signaling. Among the extracts tested, the 70% ethanol EEDK extract showed the strongest antifibrotic activity, significantly reducing LPA-induced ECM gene/protein expression and inhibiting HTM cell migration in a dose-dependent manner, whereas the 90% ethanol extract showed minimal effects. LPA robustly activated MAPK-dependent AP-1 signaling, and either pharmacologic inhibition of MAPK pathways or treatment with 70% ethanol EEDK comparably suppressed AP-1 activity and decreased downstream ECM/EMT gene expression. Thus, 70% ethanol EEDK mitigates LPA-induced TM fibrosis by inhibiting MAPK/AP-1-mediated transcription, supporting its potential as an antifibrotic strategy for glaucoma. Full article

(This article belongs to the Section Molecular Pharmacology)

► Show Figures

Figure 1

18 pages, 1244 KB

Open AccessArticle

Targeting Pediatric Glioblastomas by Combining OLIG2 Inhibitor CT-179 with Fractionated Radiation in a Panel of Patient-Derived Orthotopic Xenograft Mouse Models

by Holly Lindsay, Yuchen Du, Lin Qi, Huiyuan Zhang, Sibo Zhao, Frank K. Braun, Mari Kogiso, Clifford Stephan, Gordon Alton, Gregory Stein, Graham Beaton, Santosh Kesari, Steve Neuhauser, Tim Stearns, Jeff Chuang, Emily L. Jocoy, Carol J. Bult, Beverly Teicher, Malcolm A. Smith and Xiao-Nan Li

Int. J. Mol. Sci. 2026, 27(3), 1543; https://doi.org/10.3390/ijms27031543 - 4 Feb 2026

The poor clinical outcomes of pediatric high-grade glioma (pHGG) highlight the urgent need for new therapies. Oligodendrocyte lineage transcription factor 2 (OLIG2) is a pro-mitotic transcription factor highly expressed in glioma stem cells and may represent a novel therapeutic target. To [...] Read more.

The poor clinical outcomes of pediatric high-grade glioma (pHGG) highlight the urgent need for new therapies. Oligodendrocyte lineage transcription factor 2 (OLIG2) is a pro-mitotic transcription factor highly expressed in glioma stem cells and may represent a novel therapeutic target. To evaluate the therapeutic efficacy of an OLIG2 inhibitor CT-179 in pHGG, we determined the OLIG2 mRNA expression in 10 patient-derived orthotopic xenograft (PDOX) models. In vitro activities of CT-179 were analyzed in monolayer and neurosphere cells (0–10 µM) with and without radiation (XRT) (0–8 Gy), brain penetration was evaluated in tumor-bearing PDOX mice, and in vivo efficacy was determined at 15–240 mg/kg (oral) alone or combined with XRT (2 Gy/day × 5 days). Changes in animal survival times were analyzed using the Kaplan–Meier method, followed by pair-wise comparisons. Increased OLIG2 mRNA expression was detected in seven out of ten PDOX models. CT-179 inhibited cell viability in a time- and dose-dependent manner in all eight pGBM xenograft tumors (IC₅₀ 0.03–10 µM) and was potentiated by XRT (0.03–1 µM). Oral gavage (24 mg/kg) of CT-179 for 5 days led to effective penetration in mouse cerebrum (3232.7 ± 569.2 ng/g), cerebellum (1563.3 ± 269.6 ng/g), brain stem (1685.3 ± 309 ng/g), and PDOX tumors (1814 ± 110.3 ng/g) vs. 361.3 ± 1.5 ng/mL in serum. CT-179 alone was not active at 200 mg/kg in four models, although it was moderately effective at 240 mg/kg in one model. When combined with XRT, a significant extension of animal survival times was observed in two out of four models. Doses needed to eliminate OLIG2 expression in vitro varied from 0.3 to >1 µM in pGBM cells. In summary, our data showed that orally administered CT-179 penetrated the blood–brain barrier (BBB) and exhibited potential for inhibiting pGBM growth when combined with XRT. Full article

(This article belongs to the Special Issue Molecular Insights into Pediatric Brain Tumors: Unraveling the Complexity of Pathogenesis and Identifying New Therapeutic Targets)

► Show Figures

Figure 1

15 pages, 820 KB

Open AccessReview

Diagnostic and Therapeutic Challenges Related to HER2 Heterogeneity in Gastric Cancer: Bridging Molecular Pathology and Clinical Decision-Making

by Nelia Marina Rosanu, Lorenzo Gervaso, Renato Lobrano, Alessandro Vanoli, Chiara Alessandra Cella, Nicola Fusco and Nicola Fazio

Int. J. Mol. Sci. 2026, 27(3), 1542; https://doi.org/10.3390/ijms27031542 - 4 Feb 2026

HER2 testing represents a cornerstone of the treatment algorithm in advanced gastric and gastroesophageal junction adenocarcinoma (GC), yet its evaluation remains complex due to tumor heterogeneity and methodological variability. Unlike breast cancer, HER2 expression in GC is often incomplete and heterogeneous, resulting in [...] Read more.

HER2 testing represents a cornerstone of the treatment algorithm in advanced gastric and gastroesophageal junction adenocarcinoma (GC), yet its evaluation remains complex due to tumor heterogeneity and methodological variability. Unlike breast cancer, HER2 expression in GC is often incomplete and heterogeneous, resulting in discordant results between biopsies, resections, and metastatic sites. Both spatial and temporal HER2 heterogeneity are key determinants of testing reproducibility, diagnostic accuracy, and treatment selection and response in GC. Optimizing sampling through multiple, well-targeted biopsies, standardizing IHC/ISH protocols, and reassessing HER2 status at progression may be crucial steps to ensure diagnostic accuracy. The recognition of HER2-low disease introduces a new pathological and clinical subgroup of GC with potential sensitivity to antibody–drug conjugates, while emerging techniques such as circulating tumor DNA analysis are increasingly applied to detect HER2 amplification and co-existing genetic alterations. Integrating molecular tools and standardized reassessment strategies can enhance HER2 testing reliability and enable more precise treatment strategies, with the potential to minimize HER2 resistance mechanisms. This review provides a practice-oriented guide on the interpretation and optimization of HER2 testing in gastric cancer, while providing insight into the underlying molecular mechanisms driving heterogeneity and resistance. Full article

(This article belongs to the Collection Latest Review Papers in Molecular Oncology)

16 pages, 1588 KB

Open AccessArticle

Impact of Statin Use on Immunotherapy Outcomes and Efficacy in Non-Small Cell Lung Cancer Patients

by Alexander Yakobson, Abed Agbarya, Yulia Dudnik, Itamar Gothelf, Asmah Miari, Ronen Brenner, Ashraf Abu Jama, Nashat Abu Yasin, Abd El Nazer Dabah, Amichay Meirovitz, Natalie Maimon Rabinovich and Walid Shalata

Int. J. Mol. Sci. 2026, 27(3), 1541; https://doi.org/10.3390/ijms27031541 - 4 Feb 2026

Immune checkpoint inhibitors (ICIs) have improved outcomes in advanced non-small cell lung cancer (NSCLC). The influence of statin use, chemotherapy, PD-L1 expression, and sex on immunotherapy outcomes remains incompletely defined in real-world settings. We performed a multicenter retrospective analysis of patients with advanced [...] Read more.

Immune checkpoint inhibitors (ICIs) have improved outcomes in advanced non-small cell lung cancer (NSCLC). The influence of statin use, chemotherapy, PD-L1 expression, and sex on immunotherapy outcomes remains incompletely defined in real-world settings. We performed a multicenter retrospective analysis of patients with advanced NSCLC treated with immunotherapy-based regimens. Patients were stratified by statin exposure, chemotherapy use, PD-L1 expression (<1% vs. ≥1%), and sex. Overall survival (OS) and progression-free survival (PFS) were analyzed using Kaplan–Meier estimates and log-rank tests. Statin use was not associated with a significant OS benefit, while a numerical improvement in PFS was observed in selected subgroups. Among immunotherapy-treated patients, OS did not differ significantly by chemotherapy or statin use (median range, 19–27 months), whereas PFS differed significantly, with the longest PFS observed in patients receiving immunotherapy plus statins (26 months; p = 0.046). PD-L1 expression was the strongest determinant of outcomes, with PD-L1 ≥ 1% tumors demonstrating markedly longer OS and PFS compared with PD-L1 < 1% disease (OS up to 31 vs. 16 months; PFS up to 21 vs. 12 months; p < 0.001). No significant differences in OS or PFS were observed by sex or statin exposure (OS, 23–27 months; PFS, 14–19 months). In this real-world cohort, PD-L1 expression remained the primary predictor of survival outcomes following immunotherapy. Statin use was associated with modest PFS improvements but no consistent OS benefit, while sex did not significantly influence outcomes. These findings support continued reliance on established biomarkers and warrant prospective evaluation of statins as potential adjuncts to immunotherapy. Full article

(This article belongs to the Special Issue Advances in Targeted Therapy and Immunotherapy for Lung Cancer)

► Show Figures

Figure 1

27 pages, 4140 KB

Open AccessArticle

Characteristics of T-Cells Expressing IL-37 and Its Receptors in Inflammatory Bowel Disease

by Indiana Zorkau, Peter J. Eggenhuizen, Marie Lee, Steven X. Cho, Kylie R. James, Andrew M. Ellisdon, James C. Whisstock, Joshua D. Ooi, Marcel F. Nold, Claudia A. Nold-Petry and Rimma Goldberg

Int. J. Mol. Sci. 2026, 27(3), 1540; https://doi.org/10.3390/ijms27031540 - 4 Feb 2026

IBD pathogenesis is underpinned by an imbalance between excess inflammation caused by effector T-cells and inadequate suppression by regulatory T-cells (Tregs). Interleukin-37 (IL-37) is a potent, anti-inflammatory cytokine that signals via its receptors IL-1R5 and IL-1R8. Hence, augmenting anti-inflammatory mechanisms that drive IL-37 [...] Read more.

IBD pathogenesis is underpinned by an imbalance between excess inflammation caused by effector T-cells and inadequate suppression by regulatory T-cells (Tregs). Interleukin-37 (IL-37) is a potent, anti-inflammatory cytokine that signals via its receptors IL-1R5 and IL-1R8. Hence, augmenting anti-inflammatory mechanisms that drive IL-37 expression is a strategy to control IBD-associated inflammation. However, the role of IL-37 and its receptors in T-cells remains incompletely understood. Here, we investigated T-cell expression profiles of IL-37 and its receptors to understand the drivers of dysregulated T-cell responses in IBD and develop novel, more effective therapies. T-cell subsets from healthy control (HC), Crohn’s disease (CD) and ulcerative colitis (UC) peripheral blood mononuclear cells (PBMC) and lamina propria mononuclear cells (LPMC) were assessed for expression of IL-37 and its receptors by flow cytometry. CD3+IL-1R8+ T-cell transcriptomes underwent RNA sequencing. The phenotype and suppressive capacity of Tregs supplemented with IL-37 was assessed in vitro. Our results indicate that IL-37 and its receptors were differentially expressed among PBMC and LPMC T-cell subsets in IBD patients compared to HC. Transcription signatures unique to IBD were revealed, particularly histone and mitochondrial pathways. Remarkably, culturing Tregs with IL-37 preserved FOXP3 expression and suppressiveness at a level comparable to treatment with the well-established Treg stabilizing agent rapamycin. Altogether, our study identified differences in T-cells expressing IL-37 and its receptors that are indicative of T-cell dysfunction in IBD. These findings highlight a novel and promising avenue for restoring immune homeostasis in IBD by targeting and boosting the IL-37 signalling pathway. Full article

(This article belongs to the Special Issue Recent Molecular Research in Colitis)

32 pages, 5914 KB

Open AccessArticle

Multi-omics Analysis of a Spontaneous Type 2 Diabetes Model in Myodes rufocanus and Its Underlying Mechanisms

by Ijaz Ullah, Haseena Mujeeb, Qindan Li, Xingxuan Zhou, Habib Alam, Mujeeb Ur Rahman, Yanan Zhao, Jiazheng Zhou, Qingying Wang, Sanpin Luo, Liang Wang and Jingyu Wang

Int. J. Mol. Sci. 2026, 27(3), 1539; https://doi.org/10.3390/ijms27031539 - 4 Feb 2026

Diabetes mellitus (DM) is a chronic metabolic disorder characterized by persistent hyperglycemia, progressive β-cell dysfunction, and insulin resistance. While numerous chemically induced and transgenic rodent models exist, spontaneous models recapitulating natural type 2 diabetes mellitus (T2DM) progression remain scarce. Here, we characterize Myodes [...] Read more.

Diabetes mellitus (DM) is a chronic metabolic disorder characterized by persistent hyperglycemia, progressive β-cell dysfunction, and insulin resistance. While numerous chemically induced and transgenic rodent models exist, spontaneous models recapitulating natural type 2 diabetes mellitus (T2DM) progression remain scarce. Here, we characterize Myodes rufocanus as a novel spontaneous T2DM model through comprehensive assessments of 18-week-old male F6 voles, demonstrating hallmark diabetic features including weight gain, hyperphagia, polydipsia, hyperglycemia, insulin resistance, and dyslipidemia. Pancreatic transcriptomic profiling revealed pronounced COX14 (cytochrome c oxidase assembly factor 14) downregulation, as validated by qPCR and Western blotting in pancreatic tissue and MIN6 β-cells. MIN6 cells under chronic high-glucose conditions (30 mM) exhibited diminished mitochondrial membrane potential, impaired ATP biosynthesis, elevated reactive oxygen species, and attenuated glucose-stimulated insulin secretion, with consistent COX14 downregulation suggesting potential association with mitochondrial dysfunction. Additionally, suppressed Nrf2–HO-1 antioxidant signaling appeared to compound cellular injury, with intrinsic apoptotic pathway activation indicated by elevated Bax/Bcl-2 ratios and caspase-3 activity. These findings establish M. rufocanus as a valuable spontaneous T2DM model and implicate COX14 downregulation as a potential correlate of mitochondrial impairment and β-cell failure in diabetes pathogenesis. Full article

(This article belongs to the Special Issue Type 2 Diabetes: Molecular Pathophysiology and Treatment)

25 pages, 956 KB

Open AccessReview

SMURF2 in Anticancer Therapy: Dual Role in Carcinogenesis and Theranostics

by Joy Eom, Yejin Chun and Hae Ryung Chang

Int. J. Mol. Sci. 2026, 27(3), 1538; https://doi.org/10.3390/ijms27031538 - 4 Feb 2026

Cancer is a heterogeneous disease at the cellular level and analyzing the genetic and molecular profile is essential for targeted therapy. Cancer cells continue to mutate, often resulting in drug resistance. In addition, cancers such as triple-negative breast cancer (TNBC) lack the target [...] Read more.

Cancer is a heterogeneous disease at the cellular level and analyzing the genetic and molecular profile is essential for targeted therapy. Cancer cells continue to mutate, often resulting in drug resistance. In addition, cancers such as triple-negative breast cancer (TNBC) lack the target proteins used in some of the most effective therapies. This necessitates the identification of novel target proteins and biomarkers for effective treatment strategies. Ubiquitin E3 ligases are often differentially expressed in cancer cells, and numerous anticancer agents have been developed to inhibit them. SMURF2 is an E3 ligase that is differentially expressed in multiple cancer types. Although inhibiting upregulated SMURF2 may be strategically straightforward, enhancing the downregulated gene is often difficult. In addition, because E3 ligases ubiquitinate a variety of substrate proteins, targeting SMURF2 requires detailed analysis to achieve anticancer effect. This review discusses the dual role of SMURF2 in carcinogenesis and addresses the complex context-dependent function of SMURF2 in the various cellular pathways. In addition, resistance to existing cancer therapy related to SMURF2 and sensitivity mechanisms is discussed. Lastly, theranostic strategies for anticancer agents and biomarker development are suggested. Full article

(This article belongs to the Special Issue Innovative Strategies in the Design and Development of Anticancer Agents)

18 pages, 10431 KB

Open AccessArticle

Immunohistochemical Evidence of Telocytic Stroma Associated with Tumor Grade and Acinar Heterogeneity in Prostate Cancer

by Eduardo P. Júnior, Mário F. R. Lima, Lúcia P. F. Castro, Pablo V. N. Ramos, Juan C. M. Onofre, Rafaela S. Souza, Vivian Resende, Clémence Belleannée, Gabriel Campolina-Silva and Marcelo Mamede

Int. J. Mol. Sci. 2026, 27(3), 1537; https://doi.org/10.3390/ijms27031537 - 4 Feb 2026

Prostate cancer (PCa) progression involves dynamic interactions between neoplastic cells and the reactive stroma (RS). Although myofibroblasts are established components of the RS, the role of other stromal populations, such as telocytes, remains poorly understood. This study investigated the presence and distribution of [...] Read more.

Prostate cancer (PCa) progression involves dynamic interactions between neoplastic cells and the reactive stroma (RS). Although myofibroblasts are established components of the RS, the role of other stromal populations, such as telocytes, remains poorly understood. This study investigated the presence and distribution of a telocytic stromal phenotype (CD34⁺/Vimentin⁺) in PCa across different histological grades and acinar patterns. We used digital image analysis and standardized immunohistochemistry to assess biopsy samples from 120 patients with confirmed PCa. The telocytic phenotype showed a heterogeneous distribution and was significantly enriched in high-grade tumors and specific acinar architectures, particularly Patterns B and D. In contrast, well-differentiated regions exhibited lower telocyte density, resembling non-neoplastic prostate tissue. Although the myofibroblastic phenotype (α-SMA⁺/Vimentin⁺/CD34⁻) also increased overall with tumor grade and varied across acinar patterns, this association was comparatively weaker and less statistically robust than that observed for telocytes. These results suggest that stromal remodeling encompasses a spectrum of cellular phenotypes influenced by local architectural constraints. It is proposed that telocytes serve as key mediators of tissue organization and biomechanical signaling, contributing to a feedback loop that promotes tumor progression. Combining acinar architecture with stromal phenotyping provides a refined framework for understanding epithelial–stromal co-evolution in PCa. Full article

(This article belongs to the Special Issue Prostate Diseases: Focus on Hormone Therapies and Targeted Interventions)

► Show Figures

Figure 1

50 pages, 3024 KB

Open AccessReview

Unveiling the Therapeutic Potential of Gallic Acid: Mechanistic Insights into the Management of Pathogenesis: A Narrative Review

by Hajed Obaid A. Alharbi, Tarique Sarwar and Arshad Husain Rahmani

Int. J. Mol. Sci. 2026, 27(3), 1536; https://doi.org/10.3390/ijms27031536 - 4 Feb 2026

Gallic acid (GA) is a natural polyphenol abundantly found in a variety of fruits, including blackberries, apples, pineapples, strawberries, bananas, and grapes. With prominent anti-inflammatory and antioxidant properties, GA effectively mitigates inflammation and oxidative stress. Furthermore, it plays a significant role in modulating [...] Read more.

Gallic acid (GA) is a natural polyphenol abundantly found in a variety of fruits, including blackberries, apples, pineapples, strawberries, bananas, and grapes. With prominent anti-inflammatory and antioxidant properties, GA effectively mitigates inflammation and oxidative stress. Furthermore, it plays a significant role in modulating various cellular processes and biological activities, ultimately inhibiting the progression of pathogenesis. This review explores the multifaceted health benefits of GA, highlighting its role as antidiabetic, anti-obesity, anti-arthritis, hepatoprotective, cardioprotective, and neuroprotective effects. Additionally, its impact on the respiratory, digestive, and reproductive systems, along with its related pathogenesis, is described. Additionally, its role as an antimicrobial is defined primarily through mechanisms such as disruption of microbial cell membranes, inhibition of efflux pumps, and antibiofilm activity. Moreover, this review provides a novel, integrative analysis of GA by unifying its mechanistic roles across various pathogenesis. It further describes the role of GA in cancer management via the modulation of signaling pathways. In addition, it demonstrates the synergistic effects of GA when used in combination with other drugs/compounds and discusses nanoformulation approaches that improve its therapeutic efficacy. However, despite significant preclinical outcomes, the clinical application of GA is limited by a shortage of human trials, low bioavailability, and an inadequate understanding of its mechanisms of action and optimal dosage. To overcome these limitations, well-designed clinical trials, in vivo studies, and advanced nanoformulation approaches are required to enhance bioavailability, elucidate mechanisms of action, and increase knowledge of safety and long-term toxicity. Addressing these gaps will enable the full exploration of GA’s benefits in disease prevention and management. Full article

(This article belongs to the Special Issue Molecular Mechanisms and Therapeutic Potential of Natural Compounds)

► Show Figures

Figure 1

15 pages, 928 KB

Open AccessArticle

Neonatal Clomipramine Exposure Disrupts Epididymal Serotonin Signaling and Programs Sperm Dysfunction in Adult Rats

by Herlinda Bonilla-Jaime, Ofelia Limón-Morales, Ernesto Rodríguez-Tobón, José Edwin Mendoza-Sánchez, David Yoab Jaimes, José Luis Cortés-Altamirano, Alfonso Alfaro-Rodríguez, Marcela Arteaga-Silva, Gilberto Pérez-Sánchez, Lenin Pavón and Edith Arenas-Rios

Int. J. Mol. Sci. 2026, 27(3), 1535; https://doi.org/10.3390/ijms27031535 - 4 Feb 2026

Studies of adult depressed patients report that selective serotonin (5-HT) reuptake inhibitors (SSRIs) like clomipramine (CMI) have secondary effects on sperm quality. The epididymis possesses an autonomous serotonergic system critical for sperm maturation, whose establishment during neonatal development remains unexplored as a target [...] Read more.

Studies of adult depressed patients report that selective serotonin (5-HT) reuptake inhibitors (SSRIs) like clomipramine (CMI) have secondary effects on sperm quality. The epididymis possesses an autonomous serotonergic system critical for sperm maturation, whose establishment during neonatal development remains unexplored as a target for SSRI programming. We hypothesized that neonatal CMI exposure would disrupt the developing epididymal 5-HT system, leading to permanent sperm dysfunction. CMI (30 mg/kg s.c.) was administered to male rats between postnatal days 8–21. At 3 months, sperm from the epididymal cauda was evaluated, and 5-HT levels were measured in the testis, caput, and cauda epididymis. Our novel findings demonstrate that neonatal CMI exposure induces region-specific, long-term alterations in epididymal 5-HT levels (decreased in caput, increased in cauda) without affecting testicular 5-HT. This reprogramming of the local serotonergic milieu was associated with reduced sperm concentration, viability, normal morphology, and motility, alongside increased mitochondrial activity and reactive oxygen species. This study reveals, for the first time, that the epididymal serotonergic system is a key target for neonatal SSRI programming, providing a mechanistic link (altered 5-HT homeostasis) between early-life exposure and persistent sperm defects in adulthood. Full article

(This article belongs to the Special Issue Molecular Research on Andrology)

► Show Figures

Figure 1

32 pages, 874 KB

Open AccessReview

Advances in the Treatment of Ulcerative Colitis—From Conventional Therapies to Targeted Biologics and Small Molecules

by Aleksandra Wilk, Mateusz Pawłowski, Ewa Balcerczak, Agnieszka Jeleń, Marek Mirowski and Dagmara Szmajda-Krygier

Int. J. Mol. Sci. 2026, 27(3), 1534; https://doi.org/10.3390/ijms27031534 - 4 Feb 2026

The goals of ulcerative colitis (UC) treatment are focused on improving quality of life, achieving steroid-free remission, and minimizing the risk of cancer. In UC traditional management, a step-up strategy involves introducing increasingly more immunosuppressive medications, thus avoiding unnecessary overexposure to more potent [...] Read more.

The goals of ulcerative colitis (UC) treatment are focused on improving quality of life, achieving steroid-free remission, and minimizing the risk of cancer. In UC traditional management, a step-up strategy involves introducing increasingly more immunosuppressive medications, thus avoiding unnecessary overexposure to more potent drugs. However, in cases of severe, acute UC, priority is rapid and effective treatment to minimize the risk of complications such as bleeding, intestinal perforation, toxic megacolon or the need for colectomy. Modern approach to UC management shifts to an “accelerated step-up” or “top-down” approach in high-risk patients to prevent bowel damage. A holistic approach—integrating molecular research, clinical management and patient-centered care—enhances our understanding of disease mechanisms and therapeutic strategies, ultimately supporting improved outcomes and overall quality of life. This review aims to present the treatment options for UC along with an overview of the most modern therapies and experimental agents. Full article

(This article belongs to the Special Issue New Insights into Anticancer Strategies)

More Articles...

Submit to IJMS Review for IJMS

Journal Menu

Journal Browser

► Journal Browser

Highly Accessed Articles

View More...

Latest Books

More Books and Reprints...

E-Mail Alert

News

27 January 2026
Meet Us at the 5th Molecules Medicinal Chemistry Symposium, 14–17 May 2026, Beijing, China

22 January 2026
“Do Not Be Afraid of New Things”: Prof. Michele Parrinello on Scientific Curiosity and the Importance of Fundamental Research

3 December 2025
Meet Us at the 5th Molecules Medicinal Chemistry Symposium, 14–17 May 2026, Beijing, China

More News & Announcements...

Topics

Propose a Topic

Topic in Agrochemicals, Agronomy, Insects, IJMS, Marine Drugs, Toxins, Agriculture, Biology

Research on Natural Bioactive Product-Based Pesticidal Agents—2nd Edition Topic Editors: Min Lv, Hui Xu
Deadline: 28 February 2026

Topic in Biomedicines, Diagnostics, Endocrines, JCM, JPM, IJMS

Development of Diagnosis and Treatment Modalities in Obstetrics and Gynecology Topic Editors: Osamu Hiraike, Fuminori Taniguchi
Deadline: 20 March 2026

Topic in Cancers, IJMS, Pharmaceuticals, Pharmaceutics, Sci. Pharm., Current Oncology, Molecules

Recent Advances in Anticancer Strategies, 2nd Edition Topic Editors: Hassan Bousbaa, Zhiwei Hu
Deadline: 31 March 2026

Topic in Biomolecules, Chemistry, IJMS, Molecules, Pharmaceuticals

Progress in Drug Design: Science and Practice Topic Editors: Rui M. V. Abreu, Maria João Queiroz
Deadline: 30 April 2026

More Topics

Conferences

Propose a Conference Collaboration

11–13 March 2026 Viruses 2026 – New Horizons in Virology

8–10 July 2026 The 2nd International Online Conference on Functional Biomaterials

11–13 November 2026 The 2nd International Conference on Bioengineering: Bioengineering in an Era of AI

More Conferences...

Special Issues

Propose a Special Issue

Special Issue in IJMS

Cardiovascular Calcification: New Insights into Degenerative Mechanisms and Therapeutic Perspectives Guest Editor: Antonella Bonetti
Deadline: 10 February 2026

Special Issue in IJMS

Novel Mechanisms for the Prevention and Treatment of Stroke Guest Editor: Cesare Patrone
Deadline: 10 February 2026

Special Issue in IJMS

Current Research for Ovarian Cancer Biology and Therapeutics (Second Edition) Guest Editor: Carmela Ricciardelli
Deadline: 10 February 2026

Special Issue in IJMS

Molecular Forensics at Trial Guest Editor: Guido Viel
Deadline: 20 February 2026

More Special Issues

Topical Collections

Topical Collection in IJMS

Novel Insights into the Sleeping, Waking, and Dreaming Brain Collection Editor: Michael Lazarus

Topical Collection in IJMS

Latest Review Papers in Molecular and Cellular Biology Collection Editor: Yves Henry

Topical Collection in IJMS

Feature Papers in Molecular Oncology Collection Editors: Shailesh Singh, Peter Kuppen

Topical Collection in IJMS

State-of-the-Art Molecular Pharmacology in Italy Collection Editors: Carmine Ostacolo, Diego Guidolin, Sebastiano Mercadante, Patrizia Russo, Andrea Angeli

More Topical Collections

Back to TopTop