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Biomolecules

Biomolecules is an international, peer-reviewed, open access journal on structures and functions of bioactive and biogenic substances, molecular mechanisms with biological and medical implications as well as biomaterials and their applications, published monthly online by MDPI.

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, MEDLINE, PMC, Embase, CAPlus / SciFinder, and other databases.
Journal Rank: JCR - Q1 (Biochemistry and Molecular Biology) / CiteScore - Q1 (Biochemistry)
Rapid Publication: manuscripts are peer-reviewed and a first decision is provided to authors approximately 17.9 days after submission; acceptance to publication is undertaken in 2.9 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.
Sections: published in 15 topical sections.
Testimonials: See what our editors and authors say about Biomolecules.
Companion journal: Receptors.

Impact Factor: 4.8 (2024); 5-Year Impact Factor: 5.6 (2024)

Imprint Information Journal Flyer Open Access ISSN: 2218-273X

Latest Articles

35 pages, 17210 KB

Open AccessArticle

Phosphatidylserine Decarboxylase Regulates Retinal Ganglion Cell Neurite Outgrowth with Altered Somal Membrane Fluidics and Mitochondrial Morphology

by Sean D. Meehan, Sofia Yarosh, Victoria Pereira, Isabella Moceri and Sanjoy K. Bhattacharya

Biomolecules 2026, 16(2), 276; https://doi.org/10.3390/biom16020276 - 9 Feb 2026

Mitochondrial lipid metabolism is an emerging regulator of neuronal regeneration, yet its role remains poorly defined. We investigated the function of phosphatidylserine decarboxylase (PSD), a mitochondrial enzyme that converts phosphatidylserine to phosphatidylethanolamine (PE), in retinal ganglion cell (RGC) regeneration. Using human glaucomatous degenerating [...] Read more.

Mitochondrial lipid metabolism is an emerging regulator of neuronal regeneration, yet its role remains poorly defined. We investigated the function of phosphatidylserine decarboxylase (PSD), a mitochondrial enzyme that converts phosphatidylserine to phosphatidylethanolamine (PE), in retinal ganglion cell (RGC) regeneration. Using human glaucomatous degenerating optic nerves, we found PE was aberrantly accumulated with an elevated PSD expression and activity. In contrast, transcriptomes of regenerating RGCs present downregulated PSD, implicating PSD as a potential negative regulator of axonal growth. Using AAV2-mediated gene modulation, we evaluated how PSD knockdown (PSDKD) and PSD overexpression (PSDOE) alter RGC neurite outgrowth in vitro while evaluating effects on mitochondrial morphology, membrane fluidity by C-Laurdan staining, and lipidomes by LC-MS analysis. PSDOE did not support RGC neurite outgrowth, fragmented mitochondria, and increased polyunsaturated triacylglycerols. PSDKD significantly enhanced RGC neurite outgrowth and increased somal membrane fluidity accompanied by decreased cholesterol and saturated triacylglycerols. Notably, Doxorubicin, which attenuates PSD activity, increased neurite growth in PSDOE RGCs, supporting PSD’s activity as a negative role for growth. Using the optic nerve crush degenerative model in C57BL/6 mice, we confirm PSDKD RGCs have higher growth competency in vivo. These findings indicate PSDKD positions RGCs in a more growth-permissive state. Full article

(This article belongs to the Special Issue Biomolecular Approaches and Drugs for Neurodegeneration—2nd Edition)

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15 pages, 4939 KB

Open AccessArticle

Tricyclic Analogs of Thioguanine as Photosensitizers of Reactive Oxygen Species-Induced DNA and RNA Damage

by Katarzyna Taras-Goslinska, Katarzyna Krancewicz and Bronislaw Marciniak

Biomolecules 2026, 16(2), 275; https://doi.org/10.3390/biom16020275 - 9 Feb 2026

Analogs of tricyclic thiopurine nucleosides combine structural features of endogenous DNA adducts with efficient photosensitizing chromophores, making them valuable models for studying nucleic acid damage induced by reactive oxygen species (ROS). In this work, we investigate the photochemical properties of two tricyclic guanosine [...] Read more.

Analogs of tricyclic thiopurine nucleosides combine structural features of endogenous DNA adducts with efficient photosensitizing chromophores, making them valuable models for studying nucleic acid damage induced by reactive oxygen species (ROS). In this work, we investigate the photochemical properties of two tricyclic guanosine derivatives, 9-thio-1,N²-ethenoguanosine and 6-methyl-9-thio-1,N²-ethenoguanosine, under UVA irradiation. We characterize their excited-state behavior, their ability to generate singlet oxygen (¹O₂) and superoxide radicals (O₂^●−), and the resulting oxidative transformation pathways. Both compounds are photochemically stable under anaerobic conditions but undergo efficient oxygen-dependent phototransformation, yielding a diverse set of oxidative and dimeric photoproducts. Product analysis reveals that singlet oxygen mediates desulfurization, ring opening, and extensive sulfur oxidation, whereas radical pathways involving superoxide lead exclusively to dimer formation. Importantly, the triplet excited states of these tricyclic thiopurines are not quenched by natural nucleosides, allowing both Type I and Type II photosensitizing pathways to operate in nucleic-acid-like environments. These results provide molecular-level insight into ROS-induced purine damage and highlight tricyclic thiopurines as effective photosensitizers of oxidative DNA and RNA damage. Full article

(This article belongs to the Special Issue Molecular Mechanisms in DNA and RNA Damage and Repair)

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17 pages, 1053 KB

Open AccessArticle

Plausible Obesity-Related Chronometabolic and Nutrigenetic Nexus Concerning Dinner Glycemic Index and the FAAH C385A Variant

by Barbara Vizmanos, Alejandra Betancourt-Núñez, Erika Sierra-Ruelas, Juan José López Gómez, Daniel Rico, J. Alfredo Martínez and Daniel A. De Luis

Biomolecules 2026, 16(2), 274; https://doi.org/10.3390/biom16020274 - 9 Feb 2026

The interaction between chrono-nutrition (dinner intake), glycemic index (GI), and the C358A variant of the endocannabinoid-degrading enzyme fatty acid amide hydrolase (FAAH), along with its impact on morning fasting insulin and glycemia, has not been previously explored. This study provides new insights into [...] Read more.

The interaction between chrono-nutrition (dinner intake), glycemic index (GI), and the C358A variant of the endocannabinoid-degrading enzyme fatty acid amide hydrolase (FAAH), along with its impact on morning fasting insulin and glycemia, has not been previously explored. This study provides new insights into chronometabolic and nutrigenetic interactions. This study aims to analyze the association between the dinner GI and the C385A variant in the FAAH gene with respect to fasting glucose, insulin levels, and HOMA-IR in adults with obesity. It was hypothesized that the dinner GI, probably influenced by the FAAH variant, could be associated with glycemic homeostasis in adults with obesity. This is a secondary analysis of a cross-sectional study focused on 189 adults with obesity (129 women; mean age, 41 ± 12 years; mean BMI, 38.0 ± 5.2 kg/m²). Dietary intake was assessed through two 24 h food records, enabling the calculation of GI and macronutrient composition at each meal, especially dinner. Fasting-parameter setting and genotyping were done during the study. The lineal regression analyses were adjusted by age, sex, BMI, energy intake and dinner protein. Participants with lower fasting glucose levels had higher total GI and dinner GI values than those with higher fasting glucose levels, whereas no differences in dinner GI were observed across groups stratified by insulin or HOMA-IR levels. In fully adjusted regression models, dinner GI values remained inversely associated with fasting glucose levels (β = −0.172, 95%CI −0.298 to −0.045; p = 0.008). The FAAH C385A variant independently predicted lower insulin (β = −2.674, 95%CI −5.185 to −0.164; p = 0.037) and lower HOMA-IR (β = −0.731, 95%CI −1.364 to −0.099; p = 0.024) levels. No statistically significant interaction between dinner GI and the FAAH genotype was detected with respect to glycemia, insulin, and HOMA-IR. Overall, these findings indicate that the dinner GI influences fasting glucose levels in adults with obesity; the FAAH variant predicted lower insulin and HOMA-IR levels, supporting a plausible chrono-nutrigenetic interaction between carbohydrate quality, mealtime intake, and FAAH variation in metabolic regulation, which must be further studied. Full article

(This article belongs to the Special Issue Metabolic Inflammation and Insulin Resistance in Obesity)

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23 pages, 3691 KB

Open AccessReview

Structure, Function and Inhibition of Helicases Involved in Virus Infection

by Gisoo Sarvari and David D. Boehr

Biomolecules 2026, 16(2), 273; https://doi.org/10.3390/biom16020273 - 9 Feb 2026

Viral helicases are conserved nucleic acid-dependent ATPases that drive genome replication, gene expression, and virion assembly, thereby playing a central role in viral replication and pathogenicity. Here, we discuss structural, biochemical, and virological data to compare helicase superfamilies, their conserved motifs, and translocation [...] Read more.

Viral helicases are conserved nucleic acid-dependent ATPases that drive genome replication, gene expression, and virion assembly, thereby playing a central role in viral replication and pathogenicity. Here, we discuss structural, biochemical, and virological data to compare helicase superfamilies, their conserved motifs, and translocation models that couple ATP hydrolysis to strand separation. We then analyze how viral helicases regulate replication fork progression, transcription and translation of viral RNAs, viral genome remodeling during replication, genome-packaging strategies, and evasion of innate immune signaling. Mechanistic examples from picornaviruses, flaviviruses, herpesviruses, and coronaviruses demonstrate how helicase architecture, substrate specificity, and cofactors control these activities. Finally, we discuss the opportunities and drawbacks of targeting viral helicases with antiviral drugs, recent screening and structure-guided discovery efforts, and emerging resistance mechanisms. Overall, this review provides a virus-centered synthesis of helicase structure, function, and inhibition that links conserved enzymatic activities to diverse infection outcomes and antiviral strategies across viral families. Full article

(This article belongs to the Special Issue New Insight into the Structures and Host Cell Interactions of Emerging Viruses)

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37 pages, 2103 KB

Open AccessReview

Nuclear Receptor-Targeted Therapies: Reprogramming Metabolism with TRβ, ERRα, and LXR Modulators

by Carmen Di Giovanni and Antonio Lavecchia

Biomolecules 2026, 16(2), 272; https://doi.org/10.3390/biom16020272 - 9 Feb 2026

Metabolic disorders, including metabolic dysfunction-associated fatty liver disease (MAFLD), obesity, and dyslipidemia, impose a substantial and escalating global health burden, highlighting an urgent need for effective pharmacotherapies. Selective modulation of nuclear receptors (NRs) has emerged as a promising strategy to restore metabolic homeostasis. [...] Read more.

Metabolic disorders, including metabolic dysfunction-associated fatty liver disease (MAFLD), obesity, and dyslipidemia, impose a substantial and escalating global health burden, highlighting an urgent need for effective pharmacotherapies. Selective modulation of nuclear receptors (NRs) has emerged as a promising strategy to restore metabolic homeostasis. This review focuses on three therapeutically pivotal yet under-explored NRs: thyroid hormone receptor β (TRβ), estrogen-related receptor α (ERRα), and liver X receptor (LXRα/β). We critically examine recent advances in the development of small-molecule modulators for these targets and discuss their translational potential. TRβ agonists, including resmetirom (MGL-3196) and VK2809, have demonstrated compelling efficacy in clinical trials for metabolic dysfunction-associated steatohepatitis (MASH), significantly reducing hepatic steatosis and fibrosis. Next-generation hepatoselective modulators such as TG68 enhance tissue specificity and potency. ERRα, a master regulator of mitochondrial biogenesis and energy metabolism, is targeted by inverse agonists (compound 29, GSK5182) and agonists (JND003, SLU-PP-915), which show promise in ameliorating insulin resistance and promoting lipid oxidation in preclinical obesity models. LXRs, central players in cholesterol homeostasis, are the focus of innovative drug design aimed at harnessing atheroprotective benefits via LXRβ-selective or partial agonists, thereby circumventing adverse effects on triglyceride synthesis. Collectively, the ongoing development of TRβ, ERRα, and LXR modulators exemplifies a new frontier in precision medicine, offering powerful approaches to reprogram dysregulated metabolic pathways with substantial promise for treating metabolic diseases. Full article

(This article belongs to the Section Cellular Biochemistry)

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19 pages, 3351 KB

Open AccessPerspective

Challenges and Opportunities in Multi-Omics Data Acquisition and Analysis: Toward Integrative Solutions

by Christopher L. Hemme, Janet Atoyan, Ang Cai and Chang Liu

Biomolecules 2026, 16(2), 271; https://doi.org/10.3390/biom16020271 - 9 Feb 2026

In this perspective, we discuss the current challenges and opportunities in multi-omics, a rapidly evolving approach that integrates multiple molecular layers to advance our understanding of complex biological systems. As biomedical research moves toward precision medicine, the ability to correlate genotype, phenotype, and [...] Read more.

In this perspective, we discuss the current challenges and opportunities in multi-omics, a rapidly evolving approach that integrates multiple molecular layers to advance our understanding of complex biological systems. As biomedical research moves toward precision medicine, the ability to correlate genotype, phenotype, and environmental contexts has never been more critical. Multi-omics enhances biomarker discovery and elucidates regulatory networks underlying health and disease. The dominant scientific paradigm for over a century was to take a reductionist approach, studying individual molecular components in isolation or as simplified systems. The advent of omics technologies in the 1990s enabled a systems paradigm, allowing holistic analyses of molecular networks. These early systems studies were constrained by technology and methodology to bulk tissue measurements and single-omics analyses. Recent advances in single-cell and spatial omics, high-throughput proteomics and metabolomics, cloud computing, and artificial intelligence now allow high-resolution, spatially contextualized multi-omics analyses. Despite these gains, challenges in data analysis and interpretation remain, including high dimensionality, missing or incomplete data, multiple batch effects, and method-specific variability. Emerging strategies—such as paired data collection, staged or joint integration, and latent factor or quasi-mediation frameworks—offer promising solutions, positioning multi-omics as a transformative tool for elucidating complex mechanisms and guiding personalized medicine. Continued refinement of these approaches may further enhance the utility of multi-omics for understanding complex biological systems. Full article

(This article belongs to the Special Issue Deciphering Disease Progression Through Multi-Omics Integration)

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18 pages, 8200 KB

Open AccessArticle

Identification and Analysis of DUF506 Gene Family in Peanut (Arachis hypogaea)

by Qing Song, Gideon Asare Aboagye, Ming Liu, Ying Lan, Minghong Hu, Yanbin Hong, Renfeng Wang and Miao Chen

Biomolecules 2026, 16(2), 270; https://doi.org/10.3390/biom16020270 - 9 Feb 2026

The Domain of Unknown Function 506 (DUF506) family, part of the PD-(D/E)XK nuclease superfamily, has been shown to play a vital role in plant development and responses to abiotic stresses. However, the function of the DUF506 family in cultivated peanuts remains unknown. This [...] Read more.

The Domain of Unknown Function 506 (DUF506) family, part of the PD-(D/E)XK nuclease superfamily, has been shown to play a vital role in plant development and responses to abiotic stresses. However, the function of the DUF506 family in cultivated peanuts remains unknown. This study identified 23 AhDUF506 genes using bioinformatics approaches; these genes are spread across 15 chromosomes and grouped into 4 subfamilies. Additionally, by analyzing gene structure, upstream cis-acting elements, and transcriptional expression changes of AhDUF506 genes in different tissues and under various stress conditions, their expression levels and response mechanisms to abiotic stresses were examined. In mature tissues, the expression levels of seven AhDUF506 genes in flowers were significantly higher than those in other tissues. Under abiotic stress, their expression levels were all up-regulated in the roots of peanut plant seedlings. These findings provide an important foundation for a deeper understanding of the molecular characteristics of the DUF506 family in Arachis hypogaea (peanut), supporting future research on the functional characterization of its genes. Full article

(This article belongs to the Special Issue Plant Molecular Stress Physiology—Elucidation of Plant Responses and Defense Mechanisms Against Stress)

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20 pages, 5666 KB

Open AccessArticle

Mesenchymal Stem Cell Exosome-Mediated Delivery of Paclitaxel for Pancreatic Cancer Therapy

by Anurag Banerjee, Arpita Ghosal, Paras Mani Giri, Sakurako Tani, Yongki Choi and Buddhadev Layek

Biomolecules 2026, 16(2), 269; https://doi.org/10.3390/biom16020269 - 9 Feb 2026

Pancreatic ductal adenocarcinoma (PDAC) remains one of the most aggressive malignancies, with limited response to conventional chemotherapies such as paclitaxel (PTX) due to poor solubility, low bioavailability, and systemic toxicity. To address these limitations, this study explores mesenchymal stem cell (MSC)-derived exosomes as [...] Read more.

Pancreatic ductal adenocarcinoma (PDAC) remains one of the most aggressive malignancies, with limited response to conventional chemotherapies such as paclitaxel (PTX) due to poor solubility, low bioavailability, and systemic toxicity. To address these limitations, this study explores mesenchymal stem cell (MSC)-derived exosomes as biocompatible, tumor-homing nanocarriers for PTX delivery. Exosomes were isolated from MSC-conditioned media using ultracentrifugation and tangential flow filtration (TFF), with TFF yielding 8 to 9-fold higher exosome recovery. Flow cytometry confirmed the presence of exosomal (CD63, CD81) and MSC (CD90) surface markers, while transmission electron microscopy and dynamic light scattering revealed spherical vesicles averaging ~160 nm in diameter with a zeta potential of approximately −28 mV. PTX was loaded into exosomes using ultrasonication, achieving an encapsulation efficiency of 31.3 ± 2.0%, and release studies showed an initial burst within 24 h followed by sustained release over 7 days. Blank exosomes exhibited no cytotoxicity toward PANC-1, BxPC-3, and HPNE cells, confirming their excellent biocompatibility. In contrast, PTX-loaded exosomes significantly enhanced cytotoxicity compared to free PTX, reducing IC₅₀ values from 12.48 nM to 7.55 nM in BxPC-3 cells and from 22.44 nM to 19.29 nM in PANC-1 cells and suppressed colony formation and spheroid growth more effectively. These findings demonstrate that MSC-derived exosomes can efficiently encapsulate and deliver PTX, enhancing its antitumor efficacy. This exosome-based platform offers a promising strategy to overcome pharmacological barriers and improve therapeutic outcomes in PDAC. Full article

(This article belongs to the Special Issue Advances in Nano-Based Drug Delivery Systems)

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12 pages, 1831 KB

Open AccessArticle

One-Hour Post-Load Glucose Is Associated with Multisystem Complications in People Living with Obesity

by Ioanna Mixaki, Michalis G. Prokopakis, Georgios Dimakopoulos, Theodosios D. Filippatos, Kalliopi Kotsa and Theocharis Koufakis

Biomolecules 2026, 16(2), 268; https://doi.org/10.3390/biom16020268 - 9 Feb 2026

Background: Obesity is associated with a broad range of complications that frequently develop before the onset of type 2 diabetes mellitus (T2DM). Identifying early metabolic markers associated with such complications is essential for improving risk stratification and supporting complication-driven therapeutic strategies. Plasma glucose [...] Read more.

Background: Obesity is associated with a broad range of complications that frequently develop before the onset of type 2 diabetes mellitus (T2DM). Identifying early metabolic markers associated with such complications is essential for improving risk stratification and supporting complication-driven therapeutic strategies. Plasma glucose measured at 1 h during the oral glucose tolerance test (OGTT) has emerged as a sensitive marker of early dysglycemia and adverse cardiometabolic outcomes, but its relationship with established obesity-related complications in individuals without diabetes remains incompletely characterized. We aimed to investigate the association between 1 h post-load plasma glucose levels during OGTT and obesity-related complications in adults living with obesity without T2DM. Methods: This observational cross-sectional study included 47 adults with obesity evaluated during their first visit to obesity clinics. Individuals with T2DM or prior use of anti-obesity pharmacotherapy were excluded. All participants underwent a standard 75-g OGTT with plasma glucose and insulin measurements at fasting, 1 h, and 2 h. Obesity-related complications were recorded retrospectively through structured questionnaires, clinical assessment, and medical record review. Between-group comparisons were performed using non-parametric tests, and repeated OGTT measurements were analyzed using non-parametric longitudinal models. Results: Higher 1 h post-load glucose levels were observed in participants with arterial hypertension (p < 0.001), dyslipidemia (p = 0.020), metabolic dysfunction-associated steatotic liver disease (p = 0.005), impaired glucose tolerance (p = 0.027), obesity hypoventilation syndrome (p = 0.039), urinary incontinence (p = 0.038), and chronic kidney disease (p = 0.048). In most comparisons, 1 h post-load glucose demonstrated stronger discriminatory capacity than fasting or 2 h glucose values. Insulin levels increased markedly after glucose loading in all participants, reflecting generalized insulin resistance, but showed limited ability to discriminate between complication phenotypes. Conclusions: In people living with obesity without T2DM, elevated 1 h post-load plasma glucose during OGTT is consistently associated with multisystem obesity-related complications. These findings support the clinical relevance of 1 h post-load glucose as an integrated marker of early metabolic and systemic burden that may inform complication-driven risk stratification in obesity. Due to the observational study design, causality cannot be inferred. Full article

(This article belongs to the Section Biomacromolecules: Proteins, Nucleic Acids and Carbohydrates)

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19 pages, 1248 KB

Open AccessReview

Extracellular Vesicles: A Multidimensional Role in the Occurrence and Development of Nasopharyngeal Carcinoma

by Huining Chen, Hejing Huang and Song Qu

Biomolecules 2026, 16(2), 267; https://doi.org/10.3390/biom16020267 - 9 Feb 2026

Extracellular vesicles (EVs) have garnered significant attention in cancer research, as they enable the regulation of the occurrence, progression, and metastasis of tumors. This narrative review summarizes studies published between 2020 and 2025 from PubMed, focusing on nasopharyngeal carcinoma and extracellular vesicles. We [...] Read more.

Extracellular vesicles (EVs) have garnered significant attention in cancer research, as they enable the regulation of the occurrence, progression, and metastasis of tumors. This narrative review summarizes studies published between 2020 and 2025 from PubMed, focusing on nasopharyngeal carcinoma and extracellular vesicles. We analyze the function and mechanism of EVs in the tumor microenvironment, biomarkers, and treatment. Numerous studies have attempted to explain the mechanism of NPC-EVs affecting tumor microenvironments through the transmission of its cargo. And liquid-biopsy technology using EVs as biomarkers, such as exosomal cyclophilin A, the phosphatase and tensin homolog, and EVs-miR-30a-5p, has been studied for diagnosis and prognostic evaluation. In the therapy aspect, researchers are attempting to explore the role of EVs in the resistance process of NPC treatment, with the aim of clinical translation. Current limitations include biological distribution of EVs and so on. Future research should focus on establishing the standardized production system and more convenient separation and purification techniques for EVs. This review provides a comprehensive overview of the nasopharyngeal carcinoma-related EVs. Full article

(This article belongs to the Section Molecular Biomarkers)

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12 pages, 770 KB

Open AccessArticle

Calcitriol Modulates Both the Vitamin D Receptor and the Calcium-Sensing Receptor in Blood Mononuclear Cells in Elderly Female Patients with Hip Osteoporotic Fractures

by Javier Caballero-Villarraso, Ainoa Navarrete-Pérez, Antonio Camargo, Leo Valentín-Aragón, José Luis Gómez-Chaparro, José Manuel Quesada-Gómez and Antonio Casado-Díaz

Biomolecules 2026, 16(2), 266; https://doi.org/10.3390/biom16020266 - 8 Feb 2026

Introduction: Peripheral blood mononuclear cells (PBMCs) constitute a diverse population of cells involved in adaptive and innate immunity, playing an essential role in pathogen recognition, immune signaling, and immune response modulation. Vitamin D deficiency through the regulation of vitamin D receptor (VDR [...] Read more.

Introduction: Peripheral blood mononuclear cells (PBMCs) constitute a diverse population of cells involved in adaptive and innate immunity, playing an essential role in pathogen recognition, immune signaling, and immune response modulation. Vitamin D deficiency through the regulation of vitamin D receptor (VDR) and calcium-sensing receptor (CaSR) gene expression could influence the apoptotic functioning of PBMCs, which, despite its importance in the immune response, has not been sufficiently explored. Objectives: This research aimed to detect differences in the mRNA expression of CaSR, VDR, and apoptosis of PBMcs between elderly women with hip fractures and vitamin D deficiency and healthy young women, as well as in older women both at baseline and after administration of calcitriol. Methods: A case–control study involving 44 women (22 and 20, respectively) was conducted. The case group (hip fracture) was administered 2 µg/day of calcitriol for two weeks and a before-and-after comparison was made. The baseline gene expression of VDR and CaSR in PBMCs, as well as the effects of calcitriol on both the VDR/CaSR regulation and PBMC apoptosis, were studied in both groups. Serum bone biomarkers were also assessed. Results: No differences were observed in creatinine and calcium serum levels between the young and elderly osteoporotic women studied. Serum phosphorus and 25-hydroxyvitamin D (25(OH)D) were low in osteoporotic fractured women with vitamin D deficiency. In contrast, intact parathyroid hormone (PTH_1–84) and alkaline phosphatase were high, while no significant difference in calcitriol [l,25(OH)₂D₃] serum levels was observed. In elderly women, serum calcium, phosphorus, alkaline phosphatase, 25(OH)D, and calcitriol remained unchanged after intravenous calcitriol therapy; however, PTH_1–84 decreased after the treatment. In comparison to the young women, the elderly women showed decreased VDR and increased CaSR mRNA expression in PBMCs, as well as higher monocyte apoptosis. Conclusions: Calcitriol administration increased both VDR and CaSR mRNA expression in PBMCs and decreased PBMC apoptosis. Conclusions: The results obtained support the role of the vitamin D endocrine system as a regulator of the immune response and thus may contribute to explaining certain aspects of the immune dysfunction reported in individuals with vitamin D insufficiency. Full article

(This article belongs to the Special Issue Biochemistry and Molecular Biology of Vitamin D and Its Analog, 3rd Edition)

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33 pages, 2103 KB

Open AccessReview

Chromatin Remodeling in VSMC Phenotype Switching During Vascular Remodeling: From Mechanism to Therapeutic Potential

by Xiaozhu Ma, Shuai Mei, Qidamugai Wuyun, Li Zhou, Hu Ding and Jiangtao Yan

Biomolecules 2026, 16(2), 265; https://doi.org/10.3390/biom16020265 - 7 Feb 2026

Vascular remodeling is a characteristic pathological feature of various vascular diseases, including atherosclerosis, restenosis following vascular injury, hypertension, and aneurysms. The phenotypic switching of vascular smooth muscle cells (VSMCs) acts as a key driver of vascular remodeling. Under specific pathological stimuli, VSMCs rapidly [...] Read more.

Vascular remodeling is a characteristic pathological feature of various vascular diseases, including atherosclerosis, restenosis following vascular injury, hypertension, and aneurysms. The phenotypic switching of vascular smooth muscle cells (VSMCs) acts as a key driver of vascular remodeling. Under specific pathological stimuli, VSMCs rapidly transition from a contractile to a dedifferentiated phenotype, characterized by enhanced proliferation, migration, and secretory activity. Chromatin remodeling, a core mechanism of epigenetic regulation, orchestrates dynamic changes in chromatin structure and function through ATP-dependent remodeling complexes, histone-modifying enzymes, and DNA methyltransferases. These components collectively translate mechanical stress, metabolic disturbances, and inflammatory signals into reversible epigenetic modifications, thereby precisely regulating VSMC phenotypic switching. As such, chromatin remodeling represents a critical node for therapeutic intervention in vascular remodeling-related diseases. In recent years, a growing body of research has focused on the role of chromatin remodelers in regulating VSMC phenotype. In this review, we focus on the roles of ATP-dependent chromatin-remodeling factors and chromatin-modifying enzymes in the control of gene expression of VSMC phenotype switching. Firstly, we summarize the latest insights into chromatin remodeling and VSMC phenotypic switching, and then discuss recent advances in the identification and functional characterization of chromatin remodeling molecules, emphasizing their implications for VSMC behavior. Finally, we highlight the translational potential of targeting chromatin remodelers in the development of clinical therapies for vascular remodeling diseases and outline future directions for research in this field. Full article

(This article belongs to the Special Issue Epigenetic Regulation of Vascular Smooth Muscle Cells During Development and Disease)

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17 pages, 665 KB

Open AccessReview

Molecular Health Effects of Electronic Cigarettes

by Paweł Sutkowy, Igor Hadryś, Wiktor Gmys, Przemysław Grzempa, Aleksandra Sobieszczańska, Weronika Tuska, Karolina Błachnio and Alina Woźniak

Biomolecules 2026, 16(2), 264; https://doi.org/10.3390/biom16020264 - 7 Feb 2026

Electronic cigarettes (e-cigarettes) have emerged as a prevalent substitute for conventional cigarettes, garnering perceptions of being a safer option for health. Nicotine addicts use e-cigarettes to cease smoking. These products have also become common among young people because of their taste, smell, and [...] Read more.

Electronic cigarettes (e-cigarettes) have emerged as a prevalent substitute for conventional cigarettes, garnering perceptions of being a safer option for health. Nicotine addicts use e-cigarettes to cease smoking. These products have also become common among young people because of their taste, smell, and attractive appearance. However, accumulating experimental and clinical evidence indicates that e-cigarette use is not risk-free. The inhalation of e-cigarette aerosols exposes users and their non-using peers to a complex mixture of chemical compounds, including aldehydes, heavy metals, and flavoring agents, many of which possess pro-oxidative and pro-inflammatory properties. This review summarizes and critically analyzes current evidence on the molecular and cellular mechanisms underlying the biological effects of e-cigarette aerosols. Particular attention is given to excessive production of reactive oxygen species, mitochondrial dysfunction, DNA damage, and the activation of redox-sensitive signaling pathways, including NF-κB and NRF2. These molecular alterations may trigger acute and, with prolonged exposure, chronic oxidative stress and inflammation, which in turn can affect gene expression, protein function, and metabolic pathways. While molecular and experimental studies often demonstrate adverse biological responses to e-cigarette aerosols, the translation of these findings into long-term clinical outcomes remains an area of ongoing investigation. Full article

(This article belongs to the Section Biological Factors)

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17 pages, 12141 KB

Open AccessArticle

Chemokine Receptor Profile of Circulating Leukocyte Subsets in Response to Acute High-Intensity Interval Training

by Katharina Leuchte, Sara Fresnillo Saló, Anne Rahbech, Mikkel Byrdal, Anders Vinther and Gitte Holmen Olofsson

Biomolecules 2026, 16(2), 263; https://doi.org/10.3390/biom16020263 - 7 Feb 2026

Physically active individuals demonstrate enhanced immune competence. Efficient execution of effector function relies on chemokine receptor-regulated immune cell trafficking along chemokine gradients to sites of inflammation, infection, tumors, or tissue damage. This study investigates the impact of acute high-intensity interval training (HIIT) on [...] Read more.

Physically active individuals demonstrate enhanced immune competence. Efficient execution of effector function relies on chemokine receptor-regulated immune cell trafficking along chemokine gradients to sites of inflammation, infection, tumors, or tissue damage. This study investigates the impact of acute high-intensity interval training (HIIT) on chemokine receptor expression in leukocytes. Sixteen healthy participants completed a single HIIT session, and peripheral blood was collected before exercise (Bsl), immediately after (Ex02), and one hour later (Ex60). Surface expression of selected chemokine receptors was measured using flow cytometry on CD4⁺ T cells, γδ T cells, NK cells, and monocytes, followed by FlowSOM clustering. NK cells, CD4⁺ T cells, and γδ T cells were strongly mobilized at Ex02 and returned to or below baseline at Ex60. HIIT preferentially mobilized CX3CR1⁺ CXCR2⁺ CD56^dim NK cells, CD4⁺ T cells expressing CX3CR1^hi and CCR5⁺, and CX3CR1⁺ CD56⁺ γδ T cells, indicating mobilization of immune cells phenotypically associated with migratory and cytotoxic potential. Proportions of intermediate and non-classical monocytes increased at Ex02 and decreased at Ex60. In conclusion, HIIT induced a rapid redistribution of leukocyte subsets with chemokine receptor profiles suggesting enhanced endothelial interaction and migratory capacity toward effector tissues. Full article

(This article belongs to the Special Issue Exercise Immunology: Molecular Mechanisms and Health Applications)

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18 pages, 6817 KB

Open AccessArticle

Structural and Biophysical Analyses of Human Prostamide/Prostaglandin F Synthase with Two Active Form-Mimicking Mutations

by Sang Won Cheon, Yen Thi Kim Nguyen, Jin Mo Kang, Youngbeom Yu, Yoonyoung Heo, Hyoun Sook Kim and Byung Woo Han

Biomolecules 2026, 16(2), 262; https://doi.org/10.3390/biom16020262 - 7 Feb 2026

Human prostamide/prostaglandin F synthase (PGFS) catalyzes the NADPH-dependent conversion of prostaglandin H₂ (PGH2) to prostaglandin F₂α that plays a key role in regulating intraocular pressure and labor. Despite its physiological importance, structural and biochemical information of the human PGFS has [...] Read more.

Human prostamide/prostaglandin F synthase (PGFS) catalyzes the NADPH-dependent conversion of prostaglandin H₂ (PGH2) to prostaglandin F₂α that plays a key role in regulating intraocular pressure and labor. Despite its physiological importance, structural and biochemical information of the human PGFS has been limited because of difficulties in obtaining sufficient quality of PGFS wild-type crystal and short half-life of PGH2. Here, we report the crystal structure of human PGFS with two active site mutations, C44S/C47S double mutant (DM), which mimics the reduced active form of the CXXC motif of human PGFS. Structural analysis revealed that PGFS DM adopts a typical thioredoxin (Trx)-like fold. Analysis of B-factors and MD simulations reveals that Tyr108–Asp124 is an intrinsically flexible region, devoid of any stabilizing crystal contacts. Unlike canonical Trx-like proteins, Pro167 in PGFS adopts a trans-conformation, inducing a specific Arg40 side chain localization that creates a positive charge near the CXXC motif. Activation of PGFS by reduction of disulfide bond in the CXXC motif enhanced the thermal stability via core stabilization, yet an unexpected increase in the structural disorder was detected with CD spectroscopy, especially upon ligand binding. These findings collectively establish PGFS as a structurally distinct and redox-regulated enzyme. Our results provide novel molecular insights into PGFS as an underexplored but promising therapeutic target. Full article

(This article belongs to the Section Molecular Biophysics: Structure, Dynamics, and Function)

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11 pages, 503 KB

Open AccessArticle

Perioperative Inflammatory Cytokines in Parkinson’s Disease

by Jong-Woan Kim, Seung-ah Yoo, Yemi Choi, Gi Heon Jeong, Jaeseung Lee and Jin Joo

Biomolecules 2026, 16(2), 261; https://doi.org/10.3390/biom16020261 - 5 Feb 2026

Background: Neuroinflammation is increasingly recognized as an important contributor to Parkinson’s disease (PD), yet perioperative immune responses in this population remain incompletely characterized. This study investigated perioperative cytokine dynamics in patients with PD compared with healthy controls (HCs) undergoing orthopedic surgery under [...] Read more.

Background: Neuroinflammation is increasingly recognized as an important contributor to Parkinson’s disease (PD), yet perioperative immune responses in this population remain incompletely characterized. This study investigated perioperative cytokine dynamics in patients with PD compared with healthy controls (HCs) undergoing orthopedic surgery under general anesthesia. Methods: In this prospective pilot observational study, 50 patients scheduled for lower limb orthopedic surgery were enrolled (25 PD patients, 25 HCs). Serum cytokines (IL-6, IL-8, VEGF, MCP-1, HMGB1, S100B, and PARK7) were measured immediately after anesthesia induction (PRE) and 24 h postoperatively (POST). Between-group comparisons were performed using independent t-tests, and within-group perioperative changes were assessed using paired t-tests. Absolute (Δ = POST − PRE) and relative perioperative changes were analyzed. Results: IL-6 increased significantly after surgery in both groups, with no significant differences in absolute or relative perioperative changes between the PD and HC group. IL-8 concentrations were numerically higher in PD patients at both time points, but perioperative changes did not differ significantly between groups. VEGF decreased modestly within the PD group, whereas no significant change was observed in HCs; however, between-group differences in perioperative VEGF changes were not significant. S100B and PARK7 increased postoperatively in HCs but not in PD patients, while MCP-1 and HMGB1 showed no significant perioperative changes. Conclusions: In this pilot study, perioperative cytokine responses in patients with PD were largely comparable to those in HCs. Despite evidence of chronic low-grade inflammation in the PD group, no disease-specific amplification of acute perioperative inflammatory responses was observed. These findings suggest that perioperative immune activation in PD may be selective rather than global. Full article

17 pages, 2169 KB

Open AccessArticle

Distinct Biomarker Patterns Reveal Metabolic–Inflammatory Profiles Across Mental Disorders

by Krissia F. Godoy, Joice M. A. Rodolpho, Jaqueline Bianchi, Bruna D. L. Fragelli, Fernanda O. Duarte, Luciana Camillo, Gustavo B. Silva, Juliana A. Prado, Carlos Speglich and Fernanda F. Anibal

Biomolecules 2026, 16(2), 260; https://doi.org/10.3390/biom16020260 - 5 Feb 2026

Mental disorders, including anxiety, depression, and bipolar disorder, are frequently associated with metabolic, inflammatory, and behavioral alterations that modulate their clinical expression and increase the risk of physical comorbidities. This cross-sectional study aimed to characterize the profile of inflammatory, metabolic, and cardiac biomarkers [...] Read more.

Mental disorders, including anxiety, depression, and bipolar disorder, are frequently associated with metabolic, inflammatory, and behavioral alterations that modulate their clinical expression and increase the risk of physical comorbidities. This cross-sectional study aimed to characterize the profile of inflammatory, metabolic, and cardiac biomarkers in individuals with mental disorders compared to healthy controls, also considering anthropometric and lifestyle indicators. Fifty volunteers were evaluated and distributed into four groups: control, anxiety, depression, and bipolar disorder. All participants completed the Depression, Anxiety, and Stress Scale—21 items (DASS-21) and underwent blood collection for the assessment of inflammatory biomarkers such as C-Reactive Protein and its high-sensitivity detection (CRP/hs-CRP), Interleukins (IL-6, IL-1β) and Tumor Necrosis Factor alpha (TNF-α), metabolic biomarkers (vitamin D, cortisol, and D-dimer), and cardiac biomarkers such as N-terminal pro-B-type Natriuretic Peptide (NT-proBNP), Creatine Kinase—MB (CK-MB), troponin I (cTnI), and myoglobin (Myo). The results showed a significantly higher body mass index (BMI) in clinical groups, particularly in groups with anxiety and depression. Biomarker analyses revealed significant differences in groups with mental disorders. Elevated levels of CRP (p = 0.0038), hs-CRP (p = 0.0048), and IL-6 (p = 0.0030) were identified in the anxiety group, while the depression group was characterized by reduced vitamin D levels (p = 0.0302). Individuals with bipolar disorder presented significantly higher levels of CK-MB (p = 0.0016), CRP (p < 0.0001), IL-6 (p = 0.0198), and IL-1β (p = 0.0067). It was also observed that most individuals with mental disorders did not engage in physical activity. This inactivity was associated with worse emotional scores, higher systemic inflammation, and vitamin D deficiency. These findings reinforce the existence of an integrated axis between metabolism, inflammation, and behavior, in which excess weight, sedentary lifestyle, and nutritional deficiencies synergistically contribute to the maintenance of psychiatric symptoms and metabolic vulnerability. Integrating biomarkers, BMI, and behavioral factors may aid in identifying clinical subphenotypes and guiding more precise and individualized therapeutic strategies. Full article

(This article belongs to the Section Molecular Biomarkers)

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12 pages, 1144 KB

Open AccessArticle

Distinct Domains Contribute to the Subcellular Localization of Human cGAS in Yeast

by Sara López-Montesino, Julia María Coronas-Serna, Humberto Martín, María Molina and Víctor J. Cid

Biomolecules 2026, 16(2), 259; https://doi.org/10.3390/biom16020259 - 5 Feb 2026

Cyclic GMP-AMP synthase (cGAS) functions as a DNA sensor in the cytoplasm, triggering immune responses, but it is also translocated to the nucleus, where it is kept catalytically inactive. It consists of an unstructured N-terminal domain of around 160 amino acids, and a [...] Read more.

Cyclic GMP-AMP synthase (cGAS) functions as a DNA sensor in the cytoplasm, triggering immune responses, but it is also translocated to the nucleus, where it is kept catalytically inactive. It consists of an unstructured N-terminal domain of around 160 amino acids, and a larger C-terminal fold comprising the catalytic and DNA-binding domains. Subcellular localization of cGAS is thought to play a key role in its regulation. Here, we make use of heterologous expression in the eukaryotic model Saccharomyces cerevisiae to study cGAS localization in a neutral cellular environment. cGAS-eGFP was mostly found in aggregates at the endoplasmic reticulum–mitochondria encounter structure (ERMES) and juxtanuclear protein quality compartments (JUNQs), although some cells displayed an association between cGAS-eGFP and the plasma membrane. The N-terminus of cGAS fused to eGFP was unable to associate with the plasma membrane by itself, but its deletion dramatically promoted nuclear localization of cGAS-eGFP and decreased cytoplasmic aggregates. A mutant in the DNA-binding Zn-thumb motif of cGAS also showed a more prominent nuclear localization. Thus, both the N-terminal and C-terminal domains of cGAS seem to cooperate to prevent nuclear localization and to maintain cytoplasmic reservoirs of the protein. Heterologous cGAS expression in yeast is a valuable tool for modeling aspects of its subcellular localization and aggregative features. Full article

(This article belongs to the Section Cellular Biochemistry)

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34 pages, 970 KB

Open AccessSystematic Review

Sexually Dimorphic Neuroimmune Pathways in Chronic Pain: A Comprehensive Systematic Review of Cellular and Molecular Mechanisms

by Nebojsa Brezic, Strahinja Gligorevic, Aleksandar Sič, Vasilis-Spyridon Tseriotis and Nebojsa Nick Knezevic

Biomolecules 2026, 16(2), 258; https://doi.org/10.3390/biom16020258 - 5 Feb 2026

Chronic pain is a highly prevalent and disabling condition with a well-documented female predominance in incidence, severity and persistence. These sex differences are driven by sexually dimorphic neuroimmune mechanisms rather than psychosocial factors alone. This systematic review was conducted to comprehensively synthesize human [...] Read more.

Chronic pain is a highly prevalent and disabling condition with a well-documented female predominance in incidence, severity and persistence. These sex differences are driven by sexually dimorphic neuroimmune mechanisms rather than psychosocial factors alone. This systematic review was conducted to comprehensively synthesize human clinical and translational evidence on sex-specific neuroimmune and glial cell pathways underlying chronic pain. Scientific literature was systematically searched from database inception to December 2025 across multiple biomedical databases to identify relevant clinical and translational studies. Across pain conditions, convergent evidence demonstrated that chronic pain mechanisms diverge by sex at cellular and molecular levels. Male-predominant pathways were characterized by microglial activation, particularly P2X4 receptor–mediated signaling and brain-derived neurotrophic factor–dependent neuronal disinhibition, supported by neuroimaging, transcriptomic, and pharmacological data. In contrast, female-predominant mechanisms involved adaptive immune processes, including CD4⁺ and CD8⁺ T cell infiltration, pannexin-1–dependent leptin release, chemokine signaling, and astrocyte-mediated neuroimmune crosstalk. Sex-specific cytokine and chemokine profiles, differential glial activation patterns, and divergent neuroimmune–endocrine interactions further distinguished pain pathways between males and females. Despite consistent mechanistic trends, substantial heterogeneity within each sex, limited sex-stratified power in many studies, and variability in outcome measures constrained quantitative synthesis and generalizability. The findings indicate that chronic pain is not a unitary disorder but rather a collection of mechanistically distinct conditions shaped by biological sex. These results highlight the limitations of sex-neutral therapeutic strategies and support the development of precision medicine approaches incorporating sex-informed neuroimmune biomarkers and mechanism-matched interventions. Future studies should prioritize adequately powered sex-stratified analyses, integration of neuroimmune biomarkers and clinical trial designs capable of detecting sex-by-treatment interactions. Full article

(This article belongs to the Special Issue Endocrine, Immune and Molecular Biomarkers in Pain and Psychosomatic Disorders: Bridging Mechanisms and Medical Application)

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33 pages, 4149 KB

Open AccessReview

OGG1 and MUTYH DNA Glycosylases, the Dynamic Duo Against 8-Oxoguanine DNA Lesion: Structure, Regulation, and Novel Emerging Roles

by Ana P. Gómez-Ramírez, Melody Malek, Estela G. García-González, Sergio E. Campos, Luis G. Brieba, Sheila S. David and Carlos H. Trasviña-Arenas

Biomolecules 2026, 16(2), 257; https://doi.org/10.3390/biom16020257 - 5 Feb 2026

OGG1 and MUTYH are base excision repair (BER) DNA glycosylases (DGs) from the Helix–hairpin–Helix superfamily responsible for initiating and coordinating the repair of 8-oxo-7,8-dihydroguanine (OG), and its replication-derived mispair with adenine (OG:A), respectively. The DNA repair activities of these DGs are pivotal to [...] Read more.

OGG1 and MUTYH are base excision repair (BER) DNA glycosylases (DGs) from the Helix–hairpin–Helix superfamily responsible for initiating and coordinating the repair of 8-oxo-7,8-dihydroguanine (OG), and its replication-derived mispair with adenine (OG:A), respectively. The DNA repair activities of these DGs are pivotal to safeguarding nuclear and mitochondrial genomes. Indeed, DG functional impairment is associated with numerous pathologies, including neurodegenerative diseases, metabolic syndromes, and cancer. The timely and precise localization and processing of oxidized nucleobases carried out by these DGs are modulated by a complex regulatory network at both transcriptional and posttranslational levels, as well as intricate protein–protein interaction networks. In the absence of regulation, inappropriate and imbalanced DG activity may trigger telomeric instability, changes in transcriptional profiles and cell death. This review focuses on summarizing key features of OGG1 and MUTYH function, with a special emphasis on structure, regulation, and novel emerging roles. Full article

(This article belongs to the Special Issue Molecular Mechanisms in DNA and RNA Damage and Repair)

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