Submit to CIMB Review for CIMB Propose a Special Issue

Journal Menu

Journal Browser

Feature Papers in Molecular Medicine 2025

Special Issue Editors
Special Issue Information
Keywords
Benefits of Publishing in a Special Issue
Published Papers

A special issue of Current Issues in Molecular Biology (ISSN 1467-3045). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: closed (31 December 2025) | Viewed by 12265

Share This Special Issue

Special Issue Editors

Prof. Dr. Ru Chih C. Huang

E-Mail Website
Guest Editor

1. Department of Biology, Zanvyl Krieger School of Arts and Sciences, Johns Hopkins University, Baltimore, MD 21218-2685, USA
2. National Academy of Inventors, Tampa, FL 33612, USA
3. Academia Sinica, 128 Academia Road, Section 2, Nankang, Taipei 11529, Taiwan
Interests: chromatin structure and function; tetra-O-methyl nordihydroguaiaretic acid (M4N, terameprocol); oncogenic development in humans; chemotherapeutic drug treatments; viral replication; gene functions
Special Issues, Collections and Topics in MDPI journals

Dr. Kotohiko Kimura

E-Mail Website
Guest Editor

Department of Biology, Johns Hopkins University, 3400 N. Charles Street, Baltimore, MD 21218-2685, USA
Interests: anticancer drug; combination drug treatment; transcription factor; gene regulation; alternative splicing; cancer metabolism; mitochondria; apoptosis and hypoxia
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue, entitled “Feature Papers in Molecular Medicine 2025”, will showcase high-quality research articles, communications, and reviews in cutting-edge fields within molecular medicine.

In this Special Issue, we will highlight research that addresses many areas of this broad field and that facilitates our understanding the causes of disease on a molecular level and promotes the use of this knowledge and basic research in the prevention, diagnosis, and treatment of various diseases and disorders. We encourage the submission of manuscripts that present innovative research on physical, chemical, biological, bioinformatic, and medical techniques, focusing on molecular medicine.

Topics of interest include, but are not limited to, the following:

Identifying molecular errors in disease;
Identifying genetic errors in disease;
Molecular interventions and methodologies;
The development of novel methods of treatment/therapeutics;
Disease mechanisms;
Innovative tools and technologies;
Disease diagnostics;
Molecular mechanisms in drugs;
Molecular and medical bioinformatics;
Molecular imaging techniques.

Prof. Dr. Ru Chih C. Huang
Dr. Kotohiko Kimura
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Current Issues in Molecular Biology is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2200 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

pathogenesis
angiogenesis
autoimmune diseases
inflammatory
cancer
cardiovascular diseases
development and differentiation
endocrinology
genetics
epigenetics
hematology
hypoxia research
immunology
infectious diseases
metabolic disorders
neuroscience of diseases
regenerative medicine
prevention
therapeutics
stem cell research

Benefits of Publishing in a Special Issue

Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
Reprint: MDPI Books provides the opportunity to republish successful Special Issues in book format, both online and in print.

Further information on MDPI's Special Issue policies can be found here.

Published Papers (9 papers)

Download All Papers

Order results

Result details

Show export options Show export options

Select all

Export citation of selected articles as:

Research

Jump to: Review

12 pages, 254 KB

Open AccessArticle

Are Peripartum Changes in CCL2 Associated with Maternal Metabolic Status?

by Aleksandra Obuchowska-Standyło, Żaneta Kimber-Trojnar, Katarzyna Trojnar, Monika Czuba and Bożena Leszczyńska-Gorzelak

Curr. Issues Mol. Biol. 2026, 48(2), 143; https://doi.org/10.3390/cimb48020143 - 28 Jan 2026

Viewed by 227

Abstract

C-C motif chemokine ligand 2 (CCL2) may reflect subtle metabolic–inflammatory changes in pregnancy. This study evaluated CCL2 concentrations and their peripartum changes in women with uncomplicated term pregnancies, focusing on associations with maternal metabolic status. Serum CCL2 was measured before delivery and 48 h postpartum; urinary CCL2 was assessed postpartum. Peripartum serum change (ΔCCL2) was calculated. BMI was recorded pre-pregnancy (or early pregnancy), at delivery, and 48 h postpartum; total BMI change (ΔBMI) was derived. Participants were stratified into two groups (ΔBMI > 1 kg/m² vs. ≤1 kg/m²). Peripartum serum CCL2 changes differed significantly between ΔBMI groups. In the total cohort, CCL2 correlated with HbA1c and selected body composition indices, including fat tissue index, lean tissue index, and body cell mass. In women with ΔBMI > 1 kg/m², additional associations were found with BMI, peripartum BMI change, HbA1c, ferritin, creatinine, and total body water. Among women with ΔBMI ≤ 1 kg/m², significant relationships were observed with uric acid and triglycerides. Peripartum CCL2 dynamics appear to reflect maternal metabolic status, even in metabolically “normal” pregnancies, but these findings are exploratory and should be interpreted cautiously. CCL2 is a promising marker of subtle metabolic alterations in late pregnancy and the early postpartum period, but further validation is required before clinical application. Full article

(This article belongs to the Special Issue Feature Papers in Molecular Medicine 2025)

► Show Figures

Graphical abstract

23 pages, 12932 KB

Open AccessArticle

Collagen Type II-Targeting Lentiviral Gene Therapy for Mucopolysaccharidosis IVA

by Betul Celik, Sampurna Saikia, Shaukat Khan, Krishna Sai Musini and Shunji Tomatsu

Curr. Issues Mol. Biol. 2026, 48(1), 42; https://doi.org/10.3390/cimb48010042 - 27 Dec 2025

Viewed by 725

Abstract

Mucopolysaccharidosis (MPS IVA) is caused by pathogenic variations in the GALNS gene, leading to the accumulation of glycosaminoglycans in tissues and causing progressive skeletal lesions. While conventional lentiviral vectors (LVs) provide long-term stable expression, they do not deliver therapeutic levels to bone and cartilage. We hypothesized that engineering the LV envelope with a collagen type II-targeting peptide (WYRGRL) increases the binding affinity of the LVs for bone and cartilage. These modified vectors carrying the CBh and COL2A1 promoters delivered the GALNS gene to MPS IVA newborn mice via intravenous (IV) or intraarticular (IA) administration. The peptide-modified LVs exhibited markedly increased uptake in the liver when administered IV, but lower enzyme activity than that of the conventional vector. The modified WYRGRL-LV-COL2A1 vector elevated GALNS activity in other tissues, suggesting systemic benefits. When administered IA, the modified vectors showed potential for local treatment due to the WYRGRL peptide-mediated uptake. Additionally, there was a reduction in keratan sulfate glycosaminoglycan levels in plasma and tissues, indicating that this peptide can be a suitable candidate for disease modification. These findings pave the way for further preclinical and clinical studies, offering new possibilities for the development of targeted therapies for skeletal diseases. Full article

(This article belongs to the Special Issue Feature Papers in Molecular Medicine 2025)

► Show Figures

Figure 1

22 pages, 2679 KB

Open AccessArticle

Long-Term Liver-Targeted AAV8 Gene Therapy for Mucopolysaccharidosis IVA

by Shaukat A. Khan, Eliana Benincore-Florez, FNU Nidhi, Jose Victor Álvarez, Dione A. Holder and Shunji Tomatsu

Curr. Issues Mol. Biol. 2025, 47(11), 900; https://doi.org/10.3390/cimb47110900 - 29 Oct 2025

Cited by 1 | Viewed by 2040

Abstract

Mucopolysaccharidosis IVA (MPS IVA) is a lysosomal storage disease with an autosomal recessive trait caused by the deficiency of N-acetylgalactosamine-6-sulfate sulfatase (GALNS) enzyme, which leads to the accumulation of chondroitin-6-sulfate and keratan sulfate, primarily in cartilage and its extracellular matrix, resulting in a direct impact on cartilage and bone development, as well as subsequent systemic skeletal dysplasia. ERT and HSCT are current treatment options, but they have a limited effect on bone lesions. In this article, we investigated liver-specific AAV8 vectors with a thyroxine-binding globulin promoter in the MPS IVA murine model to evaluate the long-term (24 weeks in males and 48 weeks in females) effects of gene therapy on biochemical markers and bone pathology. Both treated groups showed GALNS enzyme activity at supraphysiological levels in plasma and in various tissues, including the liver, heart, spleen, and bone. Keratan sulfate in both groups was normalized in plasma, liver, and bone (male mice). Pathological analyses revealed a decrease in vacuolated cells in the heart muscle and valves and improvement in bone pathology in treated male mice. However, the therapeutic impact was less pronounced in treated female mice. Overall, male mice indicated a substantial improvement in biochemical parameters and pathology compared to female mice. Full article

(This article belongs to the Special Issue Feature Papers in Molecular Medicine 2025)

► Show Figures

Figure 1

23 pages, 8747 KB

Open AccessArticle

Dietary Acrylamide Induces Depression via SIRT3-Mediated Mitochondrial Oxidative Injury: Evidence from Multi-Omics and Mendelian Randomization

by Lele Zhang, Shun Li, Shengjie Liu and Zhenjie Wang

Curr. Issues Mol. Biol. 2025, 47(10), 836; https://doi.org/10.3390/cimb47100836 - 10 Oct 2025

Cited by 2 | Viewed by 1050

Abstract

Acrylamide (ACR), a common dietary pro-oxidant generated in heat-processed foods, disrupts mitochondrial redox homeostasis. While its neurotoxic effects are recognized, the role of ACR in depression remains poorly understood. We hypothesized that dietary ACR exposure promotes depression via SIRT3-dependent mitochondrial oxidative injury. Through an integrative approach combining network toxicology (to prioritize candidate targets), transcriptomics, and Mendelian randomization (MR), we identified SIRT3 as the central mediator. Molecular dynamics simulations demonstrated that ACR’s primary metabolite glycidamide (GA) formed more stable and rigid complexes with key targets (including SIRT3, TP53, CASP3, JUN, PTGS2, and PTK2) than ACR itself, as evidenced by superior structural stability, reduced flexibility, and enhanced hydrogen bonding. Transcriptomic analysis of the human prefrontal cortex (datasets GSE54567 and GSE54568) revealed mitochondrial deacetylase sirtuin 3 (SIRT3) as the most significantly suppressed gene in depression (p < 0.01), suggesting an impairment in Superoxide dismutase 2 (SOD2)-mediated antioxidant defense. MR further established JUN and PTK2 as causal genetic risk factors for depression (JUN: Odds Ratio (OR) = 1.029, 95% CI = 1.002–1.057; PTK2: OR = 1.040, 95% CI = 1.005–1.076; JUN (OR) = 1.048, 95% CI = 1.021–1.076, PTK2: OR = 1.073, 95% CI = 1.039–1.109) of each MR estimates, while other candidates lacked genetic support. Our findings demonstrate that ACR induces depression primarily through SIRT3 suppression, activating JUN/PTK2 pathways, suggesting its potential role in environmental toxicant-induced redox imbalance. Full article

(This article belongs to the Special Issue Feature Papers in Molecular Medicine 2025)

► Show Figures

Figure 1

13 pages, 1761 KB

Open AccessArticle

Association Between Body Mass Index and the Composition of Leucocyte-Poor Platelet-Rich Plasma: Implications for Personalized Approaches in Musculoskeletal Medicine

by Hadrian Platzer, Alena Bork, Malte Wellbrock, Ghazal Pourbozorg, Simone Gantz, Reza Sorbi, Ravikumar Mayakrishnan, Sébastien Hagmann, Yannic Bangert and Babak Moradi

Curr. Issues Mol. Biol. 2025, 47(10), 824; https://doi.org/10.3390/cimb47100824 - 8 Oct 2025

Cited by 1 | Viewed by 925

Abstract

Platelet-rich plasma (PRP) has gained attention in regenerative medicine due to its bio-active proteins with tissue-healing potential. However, heterogeneity in PRP composition remains a major challenge for reproducibility and standardization. Given that body mass index (BMI) affects systemic blood parameters, we investigated whether BMI affects the cellular and molecular composition of PRP. Seventy-three participants were stratified into normal weight, overweight, and obese groups. PRP was prepared using a double-syringe system, and platelet activation was induced by freeze–thaw cycles. Whole blood and PRP cell counts were analyzed, and IL6, IGF1, HGF, and PDGF-BB levels in PRP were quantified by ELISA. Platelet enrichment and levels of IGF1, HGF, and PDGF-BB in PRP did not significantly differ between BMI groups. In contrast, IL6 concentrations were higher in normal-weight compared to overweight and obese individuals. Moreover, BMI-related associations emerged between platelet counts and PDGF-BB, and between PRP proteins and sex or caffeine intake, suggesting a more complex BMI-specific modulation of PRP composition. In conclusion, our findings support considering BMI as a relevant factor in PRP therapy. Incorporating BMI into PRP standardization strategies could improve reproducibility and support personalized regenerative approaches. Full article

(This article belongs to the Special Issue Feature Papers in Molecular Medicine 2025)

► Show Figures

Figure 1

10 pages, 832 KB

Open AccessArticle

The Time of Blood Collection Does Not Alter the Composition of Leucocyte-Poor Platelet-Rich Plasma: A Quantitative Analysis of Platelets and Key Regenerative Proteins

by Hadrian Platzer, Alena Bork, Malte Wellbrock, Axel Horsch, Ghazal Pourbozorg, Simone Gantz, Reza Sorbi, Sébastien Hagmann, Yannic Bangert and Babak Moradi

Curr. Issues Mol. Biol. 2025, 47(10), 788; https://doi.org/10.3390/cimb47100788 - 23 Sep 2025

Cited by 1 | Viewed by 1626

Abstract

Platelet-rich plasma (PRP) is increasingly used in orthopedics, with its regenerative potential attributed to platelet-derived cytokines and growth factors. However, variability in PRP composition hampers standardization and reproducibility, contributing to inconsistent outcomes. Since platelet counts in whole blood follow circadian rhythms, we investigated whether blood collection time affects PRP composition. Venous blood was collected from 25 healthy individuals at 8:00 a.m., 12:00 p.m., and 4:00 p.m. Whole blood was analyzed, and leukocyte-poor PRP (LP-PRP) was prepared for quantification of erythrocytes, leukocytes, and platelets. Platelets were lysed by freeze–thaw cycles, and protein levels of PDGF-BB, IGF1, HGF, IL6, and IL10 were measured via ELISA. Whole blood exhibited diurnal variation in platelet counts. In contrast, LP-PRP was consistently depleted of leukocytes and erythrocytes and showed stable platelet enrichment (PRP/whole blood ratio 2.1 ± 0.3). Protein concentrations in LP-PRP did not differ across collection times. Despite marked interindividual variability, no time-dependent differences were observed in platelet or protein composition. These results demonstrate that LP-PRP is temporally stable, independent of blood sampling time. This robustness supports flexible clinical use and contributes to efforts toward PRP standardization in therapeutic practice. Full article

(This article belongs to the Special Issue Feature Papers in Molecular Medicine 2025)

► Show Figures

Figure 1

24 pages, 3915 KB

Open AccessArticle

Prothrombotic Genetic Mutations Are Associated with Sub-Clinical Placental Vascular Lesions: A Histopathological and Morphometric Study

by Viorela-Romina Murvai, Anca Huniadi, Radu Galiș, Gelu Florin Murvai, Timea Claudia Ghitea, Alexandra-Alina Vesa and Ioana Cristina Rotar

Curr. Issues Mol. Biol. 2025, 47(8), 612; https://doi.org/10.3390/cimb47080612 - 4 Aug 2025

Cited by 1 | Viewed by 1302

Abstract

Background: Inherited thrombophilia is increasingly recognized as a contributing factor to placental vascular pathology and adverse pregnancy outcomes. While the clinical implications are well-established, fewer studies have systematically explored the histopathological changes associated with specific genetic mutations in thrombophilic pregnancies. Materials and Methods: This retrospective observational study included two cohorts of placental samples collected between September 2020 and September 2024 at a tertiary maternity hospital. Group 1 included women diagnosed with hereditary thrombophilia, and Group 2 served as controls without known maternal pathology. Placentas were examined macroscopically and histologically, with pathologists blinded to group allocation. Histological lesions were classified according to the Amsterdam Consensus and quantified using a composite score (0–5) based on five key vascular features. Results: Placental lesions associated with maternal vascular malperfusion—including infarctions, intervillous thrombosis, stromal fibrosis, villous stasis, and acute atherosis—were significantly more frequent in the thrombophilia group (p < 0.05 for most lesions). A combination of well-established thrombophilic mutations (Factor V Leiden, Prothrombin G20210A) and other genetic polymorphisms with uncertain clinical relevance (MTHFR C677T, PAI-1 4G/4G) showed moderate-to-strong correlations with histopathological markers of placental vascular injury. A composite histological score ≥3 was significantly associated with thrombophilia (p < 0.001). Umbilical cord abnormalities, particularly altered coiling and hypertwisting, were also more prevalent in thrombophilic cases. Conclusions: Thrombophilia is associated with distinct and quantifiable placental vascular lesions, even in pregnancies without overt clinical complications. The use of a histological scoring system may aid in the retrospective identification of thrombophilia-related placental pathology and support the integration of genetic and histologic data in perinatal risk assessment. Full article

(This article belongs to the Special Issue Feature Papers in Molecular Medicine 2025)

► Show Figures

Figure 1

11 pages, 3901 KB

Open AccessArticle

A Novel Mutation in the Androgen Receptor Gene of Female Patients with 46,XY Karyotype

by Inayet Nur Uslu, Nuriye Gokce, Gulsevinc Aksoy, Nihal Inandiklioglu, Bilgin Yuksel, Munis Dundar and Osman Demirhan

Curr. Issues Mol. Biol. 2025, 47(5), 349; https://doi.org/10.3390/cimb47050349 - 10 May 2025

Cited by 1 | Viewed by 1917

Abstract

Background: In this study, we aimed to analyze androgen receptor (AR) gene mutations in five members of a family with complete androgen insensitivity syndrome (CAIS). Methods: Peripheral blood samples were collected from the proband and four relatives (mother, sister, and two aunts). Cytogenetic imaging and chromosomal analysis were per-formed to elucidate the genetic basis of the condition. Clinical Exome Sequencing (CES) was conducted to identify candidate variants, which were subsequently validated using Sanger sequencing. Evolutionary conservation analysis was performed for the identified AR gene mutation. Results: Our analyses revealed that the proband, sister, Aunt I, and Aunt II exhibited a 46,XY karyotype and carried the SRY gene. The mother, however, had a 46,XX karyotype, and did not carry the SRY gene, confirming X-linked recessive inheritance of the condition. CES results demonstrated that the proband, sister, Aunt I, and Aunt II harbored a hemizygous c.2246C>T (p.Ala749Val) mutation, while the mother carried this mutation in a heterozygous state. The presence of this mutation was confirmed by Sanger sequencing. Evolutionary conservation analysis indicated that the mutation is conserved among vertebrates. Conclusion: in conclusion, we identified a novel missense mutation (c.2246C>T) in the AR gene in five members of a CAIS-affected family, which has not been previously reported in the literature. Full article

(This article belongs to the Special Issue Feature Papers in Molecular Medicine 2025)

► Show Figures

Figure 1

Review

Jump to: Research

14 pages, 2284 KB

Open AccessReview

Senescence Modulation: An Applied Science Review of Strategies in Anti-Aging, Regenerative Aesthetics, and Oncology Therapy

by Steven Januar Kusmanto

Curr. Issues Mol. Biol. 2025, 47(12), 989; https://doi.org/10.3390/cimb47120989 - 27 Nov 2025

Viewed by 1551

Abstract

Cellular senescence is an irreversible cell cycle arrest, triggered by stressors like telomere shortening, DNA damage, and oncogenic signaling. These cells, often referred to as ‘zombie cells’ because they cease dividing yet resist apoptosis, drive the Senescence-Associated Secretory Phenotype (SASP), releasing pro-inflammatory cytokines, chemokines, growth factors, and matrix-remodeling enzymes. While senescence is a protective mechanism against malignant proliferation, its persistence in tissues contributes to aging and age-related diseases (inflammaging). Recognizing this dual role forms the basis for developing therapies that bridge anti-aging, regenerative medicine, and oncology, as precise molecular regulatory mechanisms remain incompletely understood. This review interrelates these disciplines, focusing on targeted interventions against senescent cells (SnCs). These interventions include senolytics (agents that selectively eliminate SnCs) and senomorphics (agents that suppress the SASP), offering translational insights from anti-aging/aesthetic applications into integrated treatment models. The framework addresses cancer therapeutics via immunologic modalities such as monoclonal antibodies (mAbs) and CAR T-cell therapy, alongside nucleic acid-based therapeutics (mRNA and siRNA), and is used in combination with broad-spectrum therapeutics. The novelty lies in synthesizing these disparate fields, unified by cellular senescence as a central mechanistic target. Ultimately, the goal is to identify targets that induce tumor regression, mitigate age-related vulnerabilities, promote tissue homeostasis and regeneration, and improve quality of life and overall survival. Full article

(This article belongs to the Special Issue Feature Papers in Molecular Medicine 2025)

► Show Figures

Journal Menu

Journal Browser

Feature Papers in Molecular Medicine 2025

Share This Special Issue

Special Issue Editors

Special Issue Information

Keywords

Benefits of Publishing in a Special Issue

Published Papers (9 papers)

Research

Review

Further Information

Guidelines

MDPI Initiatives

Follow MDPI