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Editor’s Choice Articles

Editor’s Choice articles are based on recommendations by the scientific editors of MDPI journals from around the world. Editors select a small number of articles recently published in the journal that they believe will be particularly interesting to readers, or important in the respective research area. The aim is to provide a snapshot of some of the most exciting work published in the various research areas of the journal.

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17 pages, 11952 KB  
Review
Microbial α-L-Rhamnosidases: Regioselective Biocatalysts for Flavonoid Biotransformation and Nutraceutical Applications
by Massimo Iorizzo
Curr. Issues Mol. Biol. 2026, 48(6), 625; https://doi.org/10.3390/cimb48060625 - 16 Jun 2026
Viewed by 234
Abstract
Microbial α-L-rhamnosidases are increasingly recognised as selective biocatalysts in food biotechnology, nutraceutical production, and health-related applications. These glycoside hydrolases catalyse the hydrolysis of terminal alpha-L-rhamnose residues from flavonoids, terpenoids, saponins, and other glycosylated natural products, thereby modulating sensory properties, solubility, intestinal absorption, and [...] Read more.
Microbial α-L-rhamnosidases are increasingly recognised as selective biocatalysts in food biotechnology, nutraceutical production, and health-related applications. These glycoside hydrolases catalyse the hydrolysis of terminal alpha-L-rhamnose residues from flavonoids, terpenoids, saponins, and other glycosylated natural products, thereby modulating sensory properties, solubility, intestinal absorption, and biological activity. While their traditional uses include debittering citrus juice and enhancing wine aroma, recent evidence demonstrates their wider value in selective flavonoid biotransformation, production of rare mono-glycosylated derivatives, probiotic fermentations, and microbiome-associated metabolism. This review summarises microbial sources, catalytic mechanisms, CAZy classification, substrate specificity, structure–function relationships, analytical methods, industrial process engineering, and emerging applications in functional foods and targeted nutraceutical applications. Particular attention is given to the distinction between alpha-(1→2)- and alpha-(1→6)-linked substrates, the production of isoquercitrin and prunin, recombinant enzyme platforms, immobilised biocatalysts, and potential future opportunities arising from metagenomics, synthetic biology, and AI-assisted protein engineering. Full article
(This article belongs to the Special Issue Latest Review Papers in Molecular Biology 2026)
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11 pages, 1308 KB  
Article
β-Hydroxybutyrate Attenuates Cardiac Inflammation and Hepatic Fibrosis in Dahl Salt-Sensitive Rats
by Satoyasu Ito, Eri Manabe, Toshiyuki Shikata, Kojiro Takamoto and Shuhei Kobuchi
Curr. Issues Mol. Biol. 2026, 48(6), 620; https://doi.org/10.3390/cimb48060620 - 16 Jun 2026
Viewed by 216
Abstract
Hypertension remains a major driver of multi-organ damage, including cardiac remodeling and hepatic complications. The ketone body β-hydroxybutyrate (BHB) has emerged as a potential metabolic signaling molecule with anti-inflammatory properties. This study investigated whether BHB attenuates cardiac stress and hepatic injury in a [...] Read more.
Hypertension remains a major driver of multi-organ damage, including cardiac remodeling and hepatic complications. The ketone body β-hydroxybutyrate (BHB) has emerged as a potential metabolic signaling molecule with anti-inflammatory properties. This study investigated whether BHB attenuates cardiac stress and hepatic injury in a salt-sensitive hypertensive model. Dahl salt-sensitive (DS) rats were fed a high-salt (HS) diet combined with a choline-deficient diet to induce cardiac inflammation and hepatic fibrosis. Rats received either BHB or a control vehicle. We found that BHB significantly suppressed hepatic lipid accumulation and fibrotic markers, including TGF-β and collagen III mRNA, even under severe dietary stress. In the heart, BHB attenuated the expression of inflammatory markers (TNF-α and ANP) despite the persistence of high systolic blood pressure. These results demonstrate that BHB exerts direct organ-protective effects through anti-inflammatory and anti-fibrotic actions that are independent of robust blood pressure reduction. Our findings suggest that BHB could be a promising metabolic intervention for managing multi-organ complications in hypertensive patients with metabolic comorbidities. Full article
(This article belongs to the Section Molecular Pharmacology)
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15 pages, 2973 KB  
Article
Zinc Complexation Overcomes the Context-Dependent Metabolic Effects of Curcumin in TNBC: Molecular Insights from TLR4/MD-2 Targeting
by Giorgia Francesca Saraceno, Gessica Bonavota, Emilia Furia, Erika Cione and Paola Tucci
Curr. Issues Mol. Biol. 2026, 48(6), 603; https://doi.org/10.3390/cimb48060603 - 6 Jun 2026
Viewed by 558
Abstract
A critical yet frequently overlooked factor is the tumor’s metabolic profile. Diabetes and chronic moderate hyperglycemia are known risk factors for triple-negative breast cancer (TNBC) that do not respond to hormonal therapy. So, identifying novel therapeutic targets and developing more effective treatments is [...] Read more.
A critical yet frequently overlooked factor is the tumor’s metabolic profile. Diabetes and chronic moderate hyperglycemia are known risk factors for triple-negative breast cancer (TNBC) that do not respond to hormonal therapy. So, identifying novel therapeutic targets and developing more effective treatments is needed. One of the key pathways involved in the aggressive nature of TNBC is the Toll-like receptor 4 (TLR4) signaling cascade. To this end, curcumin (CUR) has shown effects consistent with modulating inflammatory stress by inhibiting TLR4/MD-2. This study evaluated CUR at concentrations observed in the bloodstream (0.025–25 ng/mL) in MDA-MB-231 TNBC cells under different glucose conditions (normal, moderate, and severe hyperglycemia) and inflammatory states (LPS-induced), using cell viability assays and molecular docking. A zinc complex (Zn–CUR) was also used. Results were validated through cell viability assays. Under severe hyperglycemia, CUR unexpectedly increased cell viability in a dose-dependent manner, while Zn–CUR had no activity across all glucose levels. In LPS-induced inflammation, CUR exhibited a biphasic, dose-dependent response, being protective at mid-level doses but cytotoxic at higher doses, whereas Zn–CUR showed more consistent effects, consistent with modulation of inflammatory stress. Molecular docking suggests that Zn–CUR binds more stably within the MD-2 hydrophobic pocket than CUR, particularly when bound to LPS, with binding energies of −8.7 and −8.3 kcal/mol, respectively. However, better in silico affinity did not always translate into improved cellular effects. These findings indicate that metabolic context significantly influences CUR’s biological activity and that forming a zinc complex offers a safer, more reliable profile. This positions Zn–CUR as a candidate warranting further investigation for TNBC, particularly in the context of hyperglycemia. Full article
(This article belongs to the Special Issue Targeted Therapeutic Approaches in Cancer: Combining Natural Compounds and Conventional Drugs)
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32 pages, 2587 KB  
Review
How Polyphenol Metabolites Spatiotemporally Reprogram Transcription Factors and Human Proteostasis: A Metabolite-Centric Framework
by José Manuel Pérez de la Lastra, Celia María Curieses Andrés, Elena Bustamante Munguira, Celia Andrés Juan and Eduardo Pérez Lebeña
Curr. Issues Mol. Biol. 2026, 48(5), 529; https://doi.org/10.3390/cimb48050529 - 19 May 2026
Viewed by 462
Abstract
Polyphenols act in humans through authentic metabolites, including regio-isomeric glucuronides/sulphates, O-methylated forms, and microbiota products (urolithins, γ-valerolactones, equol), that reach targets by spatiotemporally gated exposure. Vectorial transport (MRP2/BCRP/P-gp), enterohepatic cycling, and β-glucuronidase hubs create early, surface-proximal microbursts of aglycone/catechol, whereas microbiota metabolites arrive [...] Read more.
Polyphenols act in humans through authentic metabolites, including regio-isomeric glucuronides/sulphates, O-methylated forms, and microbiota products (urolithins, γ-valerolactones, equol), that reach targets by spatiotemporally gated exposure. Vectorial transport (MRP2/BCRP/P-gp), enterohepatic cycling, and β-glucuronidase hubs create early, surface-proximal microbursts of aglycone/catechol, whereas microbiota metabolites arrive systemically 6–24 h later. Signalling emerges from a continuum of weak noncovalent modulation, conditionally gated electrophile/redox relays (catechol → o-quinone, reversible Michael adduction plus signalling-range H2O2), and PTM cascades (phosphorylation → acylation → proteostasis) that reprogram NRF2/Keap1, NF-κB/IKK, AMPK/MAPK/PI3K-Akt, SIRT1/HDACs, PPARγ, AhR, and TFEB according to where and when metabolites appear. We provide methods and standards to dose isomer-resolved metabolites at physiological free concentrations (nM-low µM) in transport-competent systems, with PK-informed sampling across seconds–minutes, 15/60/240 min, and 6–24 h, and we outline a research agenda (reference panels, spatial exposure atlases, metabotype-stratified trials, safety windows). Framed this way, polyphenols shift from vague “antioxidants” to programmable dietary signals that enable precision nutrition targeting transcription-factor and proteostasis programmes in vivo. Full article
(This article belongs to the Special Issue Mechanistic Insights into the Antioxidant Activity of Bioorganic Molecules: A Chemical Perspective)
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17 pages, 722 KB  
Perspective
Can DNA Methylation in Peritumoral and Contralateral Breast Tissue Predict Recurrence or Second Breast Cancers?
by Jennifer Hammer, Marie Malvaux, Louise van Drooghenbroeck, Cédric Van Marcke, Francois P. Duhoux and Martine Berliere
Curr. Issues Mol. Biol. 2026, 48(5), 466; https://doi.org/10.3390/cimb48050466 - 30 Apr 2026
Viewed by 540
Abstract
Despite major advances in early breast cancer detection and therapeutic strategies, locoregional and distant recurrences, as well as the development of a second primary breast cancer, remain major clinical challenges. Current prognostic tools primarily rely on tumor-specific features, such as the histological grade, [...] Read more.
Despite major advances in early breast cancer detection and therapeutic strategies, locoregional and distant recurrences, as well as the development of a second primary breast cancer, remain major clinical challenges. Current prognostic tools primarily rely on tumor-specific features, such as the histological grade, hormone receptor status, and proliferative index, and, more recently, on molecular signatures aimed at improving risk stratification and predicting recurrence. However, these approaches remain imperfect, and there is an urgent need to develop complementary strategies. Growing attention has been focused on the tumor microenvironment and the surrounding non-tumoral tissue, which may harbor clinically relevant molecular alterations. Emerging evidence suggests that DNA methylation changes can be detected in the adjacent and contralateral breast tissue and reflect early steps of carcinogenesis or predisposition to tumor development. This phenomenon, often referred to as field cancerization, raises new questions about the dynamics of cancer development. The aim of this work is to provide an integrative overview of DNA methylation alterations in normal breast tissue, including peritumoral and contralateral areas, and to examine their potential as predictive biomarkers of recurrence, based on the available data from tumoral tissue. In theory, these applications seem promising, but their role needs to be confirmed in large prospective trials, in order to overcome barriers to clinical implementation. The currently available evidence does not support a role for DNA methylation in the selection of locoregional and systemic treatment strategies, particularly with a view to reducing the rising number of uni- and bilateral mastectomies performed without any demonstrated survival benefit. Full article
(This article belongs to the Special Issue Molecular Impacts of DNA Methylation as Epigenetic Drivers of Disease Onset and Progression)
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27 pages, 8280 KB  
Review
Gla-Rich Protein (GRP): A Vitamin K-Dependent Regulator of Vascular Calcification, Inflammation, and Mineral Homeostasis
by Antun Loncaric and Lara Baticic
Curr. Issues Mol. Biol. 2026, 48(5), 458; https://doi.org/10.3390/cimb48050458 - 29 Apr 2026
Viewed by 511
Abstract
Gla-rich protein (GRP), also known as UCMA, is a vitamin K-dependent protein that has emerged as an important regulator of pathological calcification and inflammation. Vascular calcification is a major complication of chronic kidney disease and cardiovascular disorders and is now recognized as an [...] Read more.
Gla-rich protein (GRP), also known as UCMA, is a vitamin K-dependent protein that has emerged as an important regulator of pathological calcification and inflammation. Vascular calcification is a major complication of chronic kidney disease and cardiovascular disorders and is now recognized as an active and tightly regulated process rather than a passive accumulation of minerals. Increasing evidence indicates that GRP plays a protective role in mineral homeostasis through its strong calcium-binding capacity and its dependence on vitamin K-mediated gamma carboxylation. This work represents a comprehensive narrative review aimed at summarizing and critically discussing the current scientific knowledge on GRP. Available experimental and clinical data are analyzed with respect to gene expression, molecular regulation, vitamin K dependency, and underlying mechanisms of action. Particular emphasis is placed on the dual function of GRP in inhibiting ectopic calcification and modulating inflammatory responses. The evidence linking altered GRP levels or changes in its carboxylation status with chronic kidney disease, vascular calcification, calcific aortic valve disease, osteoarthritis, and tumor-associated microcalcifications is systematically examined. Current findings collectively support the concept that GRP is a multifunctional protein operating at the interface of mineral metabolism, inflammation, and tissue remodeling. Despite promising experimental data, important knowledge gaps remain, including the absence of standardized assays capable of distinguishing different GRP forms and the lack of longitudinal clinical studies evaluating its predictive value. This manuscript highlights the potential of GRP as a biomarker of disturbed mineral homeostasis and cardiovascular risk, while emphasizing the need for further research to clarify its precise biological functions and clinical relevance. Full article
(This article belongs to the Special Issue Vascular Biology in Health and Diseases)
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22 pages, 584 KB  
Review
Management of Pregnancy in Women with Inflammatory Bowel Disease: Positioning Janus Kinase Inhibitors Within Current Evidence
by Dario Colacurci, Raffaele Pellegrino, Alessia Lamart, Davide Staiano, Ilaria De Costanzo, Michele Izzo, Giuseppe Imperio, Fabio Landa, Giulia Scamardella, Enrica Di Lella, Alessandro Federico, Laura Sarno and Antonietta Gerarda Gravina
Curr. Issues Mol. Biol. 2026, 48(4), 421; https://doi.org/10.3390/cimb48040421 - 19 Apr 2026
Viewed by 1074
Abstract
Inflammatory bowel diseases (IBD) frequently affect women of reproductive age. Disease activity may arise during pregnancy, at times in severe forms, thereby generating complex clinical scenarios. Adequate control of disease activity throughout pregnancy and the achievement of a safe delivery with a healthy [...] Read more.
Inflammatory bowel diseases (IBD) frequently affect women of reproductive age. Disease activity may arise during pregnancy, at times in severe forms, thereby generating complex clinical scenarios. Adequate control of disease activity throughout pregnancy and the achievement of a safe delivery with a healthy newborn, therefore, represent vital objectives in therapeutic management. In recent years, the therapeutic armamentarium for moderate to severe IBD has expanded exponentially, with the introduction of biological agents and small molecules. However, although these therapies have largely superseded conventional treatment in complex settings, they do not share the same safety profile in pregnancy. Concerns persist regarding potential transplacental transfer and possible teratogenic effects, which justify mandatory caution in their use during pregnancy. Nonetheless, clinicians may readily encounter scenarios of active IBD during pregnancy in patients who have previously experienced failure of the biological agents most extensively studied in this context, thus necessitating an evaluation of the safety of more novel therapeutic options. This review examines the available evidence on Janus kinase inhibitors. Current data, which are highly heterogeneous and of low quality, preclude any recommendation for the use of these small molecules during pregnancy. Prospective registries and large-scale observational studies are mandatory, pending the feasibility of dedicated trials, to better characterise these inhibitors, which could prove valuable, should the evidence ultimately support their use, in women with biologic multi-failure active IBD during pregnancy. Full article
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17 pages, 5435 KB  
Article
Curcumin Attenuates LPS-Induced Migration/EMT and LPS/ATP-Associated IL-1β Release in Androgen-Independent Prostate Cancer Cells
by Mon-Der Cho, Shang-Yu Chou, Yu-Ming Hsu, Chi-Ying Li, Yi-Hong Tsai and Fang-Rong Chang
Curr. Issues Mol. Biol. 2026, 48(4), 413; https://doi.org/10.3390/cimb48040413 - 17 Apr 2026
Viewed by 681
Abstract
Inflammation can promote aggressive phenotypes in prostate cancer, including enhanced migration/EMT-like changes and inflammasome-associated cytokine release. Here, we examined whether curcumin modulates these inflammation-driven responses in androgen-independent prostate cancer cells. PC-3 and DU145 cells were treated with curcumin (10 or 25 μM) or [...] Read more.
Inflammation can promote aggressive phenotypes in prostate cancer, including enhanced migration/EMT-like changes and inflammasome-associated cytokine release. Here, we examined whether curcumin modulates these inflammation-driven responses in androgen-independent prostate cancer cells. PC-3 and DU145 cells were treated with curcumin (10 or 25 μM) or N-acetylcysteine (NAC; 2 mM). Sub-cytotoxic dosing was defined by CCK-8 viability assays. LPS (0.5 μg/mL) was used to induce motility-, invasion-, and EMT-associated responses, assessed by wound-healing assay, Matrigel-coated Transwell invasion assay, and RT–qPCR of SNAI1, CDH1, and VIM. Intracellular ROS was quantified by CM-H2DCFDA flow cytometry. Inflammasome-associated and EMT-related protein changes were evaluated under LPS priming (24 h) followed by ATP triggering (5 mM, 1 h), with NLRP3, cleaved caspase-1, cleaved IL-1β, vimentin, and E-cadherin assessed by immunoblotting and IL-1β secretion measured by ELISA. Curcumin at 10–25 μM did not cause overt cytotoxicity and significantly reduced LPS-induced wound closure and invasive activity in both cell lines, accompanied by attenuation of EMT-associated transcriptional changes and a decrease in ROS-positive events. Under LPS priming/ATP triggering, inflammasome-associated protein signals and IL-1β secretion were robustly induced; curcumin suppressed IL-1β release and attenuated NLRP3, cleaved caspase-1, and cleaved IL-1β signals, while reversing vimentin/E-cadherin changes. NAC produced similar inhibitory patterns, supporting a redox-linked contribution to these responses. Collectively, curcumin dampens inflammation-driven motility/invasion, EMT-associated changes, and inflammasome-associated responses in androgen-independent prostate cancer cells. Full article
(This article belongs to the Section Bioorganic Chemistry and Medicinal Chemistry)
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15 pages, 1206 KB  
Article
Treatment of Mesenchymal Stem Cell-Derived Extracellular Vesicles with Extract of Cultured Lentinula edodes Modulates Breast Cancer Stem Cells and MicroRNA Reprogramming
by Farzaneh Sharifzad, Nawal Alsadi, Hamed Yasavoli-Sharahi, Roghayeh Shahbazi, Dylan Burger and Chantal Matar
Curr. Issues Mol. Biol. 2026, 48(4), 368; https://doi.org/10.3390/cimb48040368 - 1 Apr 2026
Viewed by 906
Abstract
Breast carcinoma represents the most frequent malignancy in women in Canada, and intrinsic or acquired drug resistance significantly increases the risk of recurrence and metastasis. Although front-line therapy is multimodal, chemoresistance remains a major hurdle in treatment and therapy, and the intake of [...] Read more.
Breast carcinoma represents the most frequent malignancy in women in Canada, and intrinsic or acquired drug resistance significantly increases the risk of recurrence and metastasis. Although front-line therapy is multimodal, chemoresistance remains a major hurdle in treatment and therapy, and the intake of natural compounds resulting from fermentation processes is currently considered an effective strategy to overcome this problem. This study investigated the effect of extracellular vesicles (EVs) from Mesenchymal Stromal/stem cells (MSCs) pretreated with cultured Lentinula edodes extract (AHCC) on reducing chemoresistance and modulating microRNAs in the MCF-7 and MCF-7/DOX cell lines. EV characterization was performed using nanoparticle tracking analysis, and microRNAs and the formation of cancer stem cells were studied. The miRNA analysis revealed that AHCC significantly downregulated oncogenic miR-155 but upregulated the tumor-suppressive microRNAs miR-34a, miR-Let7a, and miR-200c. In vitro experiments showed inhibition of cancer stem cell proliferation after challenging the cells with AHCC-pretreated EVs. Conclusion: Our data demonstrated that AHCC may contribute to modulation of the tumor microenvironment, thus influencing the development of cancer stem cells. Full article
(This article belongs to the Special Issue Targeted Therapeutic Approaches in Cancer: Combining Natural Compounds and Conventional Drugs)
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26 pages, 1342 KB  
Review
Current and Developing Therapeutics for Dry Eye Disease: Targeting Ion Channels
by Rebecca Jung, Emily Kao, Victor H. Guaiquil, Ali R. Djalilian and Mark I. Rosenblatt
Curr. Issues Mol. Biol. 2026, 48(3), 332; https://doi.org/10.3390/cimb48030332 - 21 Mar 2026
Cited by 1 | Viewed by 1620
Abstract
Dry eye disease (DED) is an ocular surface disorder characterized by tear film instability, inflammation, epithelial damage, and neurosensory abnormalities. Due to its multifactorial etiology and pathophysiology, conventional therapies that focus on lubrication and immunosuppression often fall short in addressing the neuropathic component [...] Read more.
Dry eye disease (DED) is an ocular surface disorder characterized by tear film instability, inflammation, epithelial damage, and neurosensory abnormalities. Due to its multifactorial etiology and pathophysiology, conventional therapies that focus on lubrication and immunosuppression often fall short in addressing the neuropathic component of ocular pain experienced by a growing subset of patients. Recent developments in sensory neuroscience have highlighted the pivotal role of ion channels in mediating ocular surface homeostasis, pain signaling, and inflammation. This review examines the role of the following major ion channel families in the pathophysiology of DED and neuropathic ocular pain: transient receptor potential (TRP) channels, voltage-gated sodium (Nav) channels, and purinergic P2X receptors. The review details their anatomical distribution, molecular function, and responses to environmental stimuli such as heat, cold, osmolarity, and injury. Current treatments, such as artificial tears, anti-inflammatory drops, and systemic neuromodulators, are also reviewed in relation to their effects on ion channel modulation. Additionally, emerging therapies that directly target sensory transduction pathways are introduced. This review highlights the therapeutic potential of ion channel modulation in personalizing treatment for patients with ocular surface pain, particularly those with neuropathic features unresponsive to standard care. Full article
(This article belongs to the Special Issue Latest Review Papers in Molecular Biology 2026)
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20 pages, 1827 KB  
Article
Effects of Citicoline-Based Supplementation on Lipid Peroxidation Markers and Sirtuin-1 Expression in Ischemic Stroke
by Todorka Sokrateva, Bogdan Roussev, Daniela V. Vankova, Deyana G. Vankova, Diana Ivanova, Mihael Tsalta-Mladenov, Darina Georgieva, Miglena N. Nikolova, Galya Mihaylova and Milka A. Nashar
Curr. Issues Mol. Biol. 2026, 48(3), 314; https://doi.org/10.3390/cimb48030314 - 15 Mar 2026
Cited by 1 | Viewed by 1342
Abstract
Ischemic stroke (IS) is associated with pronounced oxidative stress and lipid peroxidation, which contribute to secondary neuronal damage. This study explored the effects of a six-month intervention with a new formulation containing citicoline, vitamin C, and extracts from green tea and aronia (Cytodeox™) [...] Read more.
Ischemic stroke (IS) is associated with pronounced oxidative stress and lipid peroxidation, which contribute to secondary neuronal damage. This study explored the effects of a six-month intervention with a new formulation containing citicoline, vitamin C, and extracts from green tea and aronia (Cytodeox™) on arachidonic acid (AA) metabolism, lipid peroxidation assessed by total 8-iso-prostaglandin F2α (8-iso-PGF2α), and Sirtuin-1 (SIRT1) expression in healthy controls (n = 43) and patients with IS (n = 53), both with and without comorbidities. AA and 8-iso-PGF2α were quantified in serum using UPLC–MS and ELISA, respectively, and the fold change in SIRT1 expression was assessed in peripheral blood mononuclear cells (PBMCs) by RT-qPCR. In healthy controls, Cytodeox™ significantly lowered AA and 8-iso-PGF2α levels. IS patients showed markedly increased baseline 8-iso-PGF2α, indicating severe oxidative stress. Following supplementation, 8-iso-PGF2α levels increased in patients with comorbidities, particularly diabetes mellitus (DM), whereas an exploratory analysis suggested a decreasing trend in patients without comorbidities. SIRT1 expression was significantly upregulated in IS patients, with the most pronounced increase observed in the DM subgroup, while remaining unchanged in controls. These findings suggest a protective, antioxidant, and membrane stabilising effect of Cytodeox™ under conditions of preserved or moderately impaired redox homeostasis, supporting its potential role as a preventive or early supportive intervention. Full article
(This article belongs to the Special Issue Repurposing and Innovation: Drug Research in Neuroprotection)
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12 pages, 3941 KB  
Article
A Novel Anti-Cadherin-19 Monoclonal Antibody (Ca19Mab-8) for Flow Cytometry, Western Blotting, and Immunohistochemistry
by Guanjie Li, Hiroyuki Suzuki, Mika K. Kaneko and Yukinari Kato
Curr. Issues Mol. Biol. 2026, 48(3), 307; https://doi.org/10.3390/cimb48030307 - 12 Mar 2026
Viewed by 682
Abstract
The type II cadherin Cadherin-19 (CDH19) plays a crucial role in neural crest development. CDH19 regulates cell–cell junctions and migration by forming catenin–cytoskeleton complexes. Although anti-CDH19 monoclonal antibodies (mAbs) are used for specific applications such as Western blotting and immunohistochemistry (IHC), suitable anti-CDH19 [...] Read more.
The type II cadherin Cadherin-19 (CDH19) plays a crucial role in neural crest development. CDH19 regulates cell–cell junctions and migration by forming catenin–cytoskeleton complexes. Although anti-CDH19 monoclonal antibodies (mAbs) are used for specific applications such as Western blotting and immunohistochemistry (IHC), suitable anti-CDH19 mAbs for flow cytometry are limited. Therefore, developing mAbs that specifically recognize cell-surface-expressed CDH19 is essential for advancing both basic research and therapeutic strategies. Here, novel anti-human CDH19 mAbs (Ca19Mabs) were created using flow cytometry-based high-throughput screening. One clone, Ca19Mab-8 (IgG1, κ), specifically recognized CDH19-overexpressed Chinese hamster ovary-K1 cells but did not bind to other 21 CDHs (including both type I and type II CDHs) in flow cytometry. Additionally, Ca19Mab-8 recognized endogenous CDH19 in the human glioblastoma cell line LN229. The dissociation constant (KD) of Ca19Mab-8 for LN229/CDH19 was 9.0 × 10−9 M. Ca19Mab-8 also detected endogenous CDH19 in Western blotting. Furthermore, Ca19Mab-8 can detect CDH19 in IHC using human melanoma tissue. These findings suggest that Ca19Mab-8 is a novel mAb that detects cell-surface-expressed CDH19 with high specificity and is suitable for various applications in basic research. Therefore, Ca19Mab-8 has potential for clinical diagnosis and tumor therapy. Full article
(This article belongs to the Topic Autism: Molecular Bases, Diagnosis and Therapies, 3rd Edition)
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22 pages, 2019 KB  
Article
Physicochemical and Proteolytic Barriers Limiting Activity of Cpl-1 and Pal Endolysins in Human Circulation
by Marek Adam Harhala, Katarzyna Gembara, Izabela Rybicka, Zuzanna Maria Kaźmierczak, Paulina Miernikiewicz and Krystyna Dąbrowska
Curr. Issues Mol. Biol. 2026, 48(2), 231; https://doi.org/10.3390/cimb48020231 - 21 Feb 2026
Viewed by 923
Abstract
The growing prevalence of antibiotic-resistant bacterial infections poses a serious burden on healthcare systems worldwide. Endolysins are promising candidates for a new type of antibiotic due to their strong bacteriolytic activity. However, important limitations, including reduced activity and short persistence in the bloodstream, [...] Read more.
The growing prevalence of antibiotic-resistant bacterial infections poses a serious burden on healthcare systems worldwide. Endolysins are promising candidates for a new type of antibiotic due to their strong bacteriolytic activity. However, important limitations, including reduced activity and short persistence in the bloodstream, must still be addressed. We evaluated the key physicochemical and biological factors limiting the activity and stability of the endolysins Cpl-1 and Pal in blood. The analysis included ionic composition and strength, pH, bystander proteins, physiological temperature, and proteolytic activity. Our results indicate that the aforementioned factors significantly affect Cpl-1 and Pal, suggesting that physiological conditions in human circulation markedly restrict the anti-bacterial potential of endolysins. To overcome these limitations, we designed a set of Cpl-1 and Pal variants with modified amino acid compositions aimed at increasing their resistance to such physiological constraints. One variant demonstrated improved performance in an ex vivo mouse model and lacked a cleavage site for blood proteases. Full article
(This article belongs to the Section Biochemistry, Molecular and Cellular Biology)
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45 pages, 1122 KB  
Review
Phytochemical Quorum-Sensing Inhibitors Against Bacterial Pathogens: Mechanisms of Action and Translational Challenges
by Christos Papaneophytou
Curr. Issues Mol. Biol. 2026, 48(2), 214; https://doi.org/10.3390/cimb48020214 - 14 Feb 2026
Cited by 6 | Viewed by 1837
Abstract
Antimicrobial resistance is a critical global health challenge, driven by the rapid emergence of multidrug-resistant bacterial pathogens and exacerbated by extensive antibiotic use, which imposes intense selective pressure and disrupts host-associated microbial communities. In this context, quorum sensing (QS), a conserved molecular communication [...] Read more.
Antimicrobial resistance is a critical global health challenge, driven by the rapid emergence of multidrug-resistant bacterial pathogens and exacerbated by extensive antibiotic use, which imposes intense selective pressure and disrupts host-associated microbial communities. In this context, quorum sensing (QS), a conserved molecular communication system that coordinates population-level gene regulation, virulence expression, and biofilm development, has emerged as an attractive target for anti-virulence intervention. A growing body of evidence indicates that phytochemicals, such as curcumin, carvacrol, carnosol, eugenol, and chlorogenic acid, can modulate key QS pathways, including acyl-homoserine lactone-, autoinducing peptide-, and LuxS/AI-2-mediated signaling, thereby attenuating pathogenic behaviors at sub-inhibitory concentrations that do not directly impair bacterial viability. Despite this promise, the translational development of phytochemical-based QS inhibitors remains limited. Because QS also regulates cooperative and homeostatic functions in beneficial bacteria, QS-targeted interventions raise concerns about microbiome disruption and ecological imbalance. Furthermore, the literature is marked by substantial methodological heterogeneity, reliance on indirect phenotypic endpoints, limited molecular target validation, and insufficient assessment of toxicity, bioavailability, and pharmacokinetics. The predominance of simplified in vitro models further constrains extrapolation to complex host-associated and polymicrobial environments. This review critically examines the molecular mechanisms underlying phytochemical modulation of bacterial QS, synthesizes pathogen-focused experimental evidence, and evaluates key translational challenges arising from QS conservation, microbiome considerations, and methodological limitations. Addressing these barriers through mechanism-resolved experimentation, standardized evaluation frameworks, and microbiome-aware testing strategies will be essential for advancing phytochemical QS inhibitors toward clinically and industrially relevant anti-virulence applications. Full article
(This article belongs to the Special Issue Advances in Phytochemical Research: Molecular Pathways in Health and Disease)
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14 pages, 1726 KB  
Article
Rhus coriaria Linn Extract as a Natural Inhibitor of Influenza A Virus Replication In Vitro
by Carla Prezioso, Maria Luisa Savo Sardaro, Flavio Frezza, Dolores Limongi, Salvatore Velotto, Leonardo Lupacchini, Giovanni D’Auria, Marta De Angelis, Lucia Nencioni and Paola Checconi
Curr. Issues Mol. Biol. 2026, 48(2), 207; https://doi.org/10.3390/cimb48020207 - 13 Feb 2026
Viewed by 987
Abstract
Influenza A viruses remain a major public health threat due to their high mutation rates, antigenic variability, and the emergence of resistance to current antivirals, underscoring the need for novel therapeutic options. Natural compounds rich in polyphenols and flavonoids have attracted increasing attention [...] Read more.
Influenza A viruses remain a major public health threat due to their high mutation rates, antigenic variability, and the emergence of resistance to current antivirals, underscoring the need for novel therapeutic options. Natural compounds rich in polyphenols and flavonoids have attracted increasing attention as potential broad-spectrum antiviral agents. In this study, the activity of Rhus coriaria L. water extract against Influenza A virus in BEAS-2B human bronchial epithelial cells was investigated. Cell viability assay identified non-cytotoxic concentrations, up to 0.1 mg/mL, which were used in infection experiments. Viral replication was assessed at multiple levels by quantitative real-time PCR, western blotting, immunofluorescence and tissue culture infectious dose 50% (TCID50). Treatment with R. coriaria extract resulted in a dose-dependent and statistically significant reduction of viral load. The extract decreased mRNA levels of Hemagglutin (HA), Neuraminidase (NA) and Matrix protein 2 (M2). Consistently, western blot analysis showed a decrease in major viral proteins HA, Nucleoprotein (NP), Matrix protein 1 (M1) and Polymerase Acidic protein (PA). Confocal images revealed a marked reduction in HA and PA signals, results that are statistically significant according to quantitative fluorescence evaluation. The convergence of results obtained through independent methodologies at both the transcriptional and protein levels highlight the robustness of the findings. These data provide the experimental evidence that Rhus coriaria interferes with influenza A virus replication in airway epithelial cells and support its further investigation as a promising phytochemical platform for the development of novel anti-influenza strategies. Full article
(This article belongs to the Special Issue Molecular and Real-World Evidence Research of Respiratory Diseases and Infections, 2nd Edition)
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22 pages, 2522 KB  
Article
Oncological Safety of High Hydrostatic Pressure Treatment: Effects on Cancer-Associated Fibroblast-like Transdifferentiation of Adipose Stromal Cells
by Julia Kristin Brach, Vivica Freiin Grote, Anika Jonitz-Heincke, Rainer Bader, Daniel Strüder, Marco Hoffmann, Sven Gerlach, Petra Fischer, Markus Wirth, Tim Ruhl, Justus P. Beier, Agmal Scherzad and Stephan Hackenberg
Curr. Issues Mol. Biol. 2026, 48(1), 91; https://doi.org/10.3390/cimb48010091 - 16 Jan 2026
Viewed by 1056
Abstract
Oncological safety is essential for autologous reconstruction after resection of cartilage-infiltrating head and neck tumors. High hydrostatic pressure (HHP) enables complete devitalization of tumor-infiltrated tissue while preserving extracellular matrix integrity. However, residual soluble tumor-derived products may influence infiltrating stromal cells. This study examined [...] Read more.
Oncological safety is essential for autologous reconstruction after resection of cartilage-infiltrating head and neck tumors. High hydrostatic pressure (HHP) enables complete devitalization of tumor-infiltrated tissue while preserving extracellular matrix integrity. However, residual soluble tumor-derived products may influence infiltrating stromal cells. This study examined whether conditioned media (CM) from HHP-treated head and neck squamous cell carcinoma (HNSCC) cells induce cancer-associated fibroblast (CAF)-like transdifferentiation of human adipose stromal cells (hASCs). HASCs were exposed to CM from untreated or HHP-treated (300 MPa) HNSCC cells, tumor-CM (TCM), or TGF-β1. Morphological changes in hASCs were evaluated, and CAF marker expression was analyzed by qRT-PCR, immunofluorescence, Western blot, and ELISA. Cytokines were quantified via multiplex analysis. TGF-β1 induced a CAF-like phenotype with α-SMA upregulation, whereas TCM and 0 MPa-CM caused only modest increases in selected markers. Although 300 MPa-CM did not induce CAF-associated molecular signatures, hASCs exhibited morphological alterations, underscoring that morphology alone is insufficient to define CAF transdifferentiation. Cytokine secretion was elevated in response to all CM conditions. These findings indicate that HHP treatment at 300 MPa abolishes the paracrine CAF-inducing potential of tumor-derived mediators in vitro, supporting the oncological safety of HHP-treated tissues under these experimental condition, although further in vivo validation is warranted Full article
(This article belongs to the Section Molecular Medicine)
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16 pages, 1175 KB  
Article
HERVs and Epigenetic Regulators Transcriptional Expression After Chondrogenic Differentiation of Adipose Tissue-Derived Mesenchymal Stem Cells
by Ilaria Galliano, Cristina Calvi, Stefano Gambarino, Alice Dato, Anna Pau, Maddalena Dini, Anna Clemente, Carlotta Castagnoli and Massimiliano Bergallo
Curr. Issues Mol. Biol. 2026, 48(1), 37; https://doi.org/10.3390/cimb48010037 - 26 Dec 2025
Viewed by 612
Abstract
Mesenchymal stem cells (MSCs) are multipotent cells capable of differentiating into various connective tissue cell types. Adipose tissue provides a rich source of MSCs (ADSCs), which can differentiate into osteoblasts, adipocytes, and chondroblasts. Pluripotency factors such as SOX2, NANOG, and OCT4 maintain MSC [...] Read more.
Mesenchymal stem cells (MSCs) are multipotent cells capable of differentiating into various connective tissue cell types. Adipose tissue provides a rich source of MSCs (ADSCs), which can differentiate into osteoblasts, adipocytes, and chondroblasts. Pluripotency factors such as SOX2, NANOG, and OCT4 maintain MSC stemness, whereas human endogenous retroviruses (HERVs) and their epigenetic regulators TRIM28 and SETDB1 have been implicated in transcriptional regulation and cell fate decisions. This study investigated the transcriptional expression of HERV-H, -K, and -W, TRIM28, SETDB1, and pluripotency markers (NANOG, OCT4, SOX2) during chondrogenic differentiation of ADSCs using Real-Time PCR. Chondrogenesis was confirmed by aggrecan (ACAN) upregulation and aggrecan immunostaining. Although no statistically significant differences were observed for HERV-H, HERV-K, or HERV-W, HERV-K and HERV-W showed a trend toward decreased expression in differentiated cells, consistent with the overall shift in transcriptional profile during lineage commitment. TRIM28 expression was significantly reduced, while SETDB1 showed a decreasing trend. Among pluripotency markers, OCT4 was significantly downregulated, whereas NANOG and SOX2 remained stable. Correlation analyses revealed that in differentiated ADSCs, HERV-W expression correlated negatively with TRIM28 and positively with SETDB1, while no correlations were found for HERV-H or HERV-K. These findings suggest that specific HERV families and their epigenetic regulators may undergo coordinated modulation during chondrogenic differentiation, supporting a complex and family-specific interplay between retroelement regulation, pluripotency factors, and MSC lineage commitment. Full article
(This article belongs to the Special Issue Innovative Approaches in Bone and Cartilage Regeneration: From Stem Cells to Organoids)
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19 pages, 5171 KB  
Article
Interferon-Type-I Response and Autophagy Independently Regulate Radiation-Induced HLA-Class-I Molecule Expression in Lung Cancer
by Erasmia T. Xanthopoulou, Ioannis Lamprou, Ioannis M. Koukourakis, Achilleas G. Mitrakas, Georgios D. Michos, Anastasia Polyzoidou, Filippos G. Antoniadis, Alexandra Giatromanolaki and Michael I. Koukourakis
Curr. Issues Mol. Biol. 2026, 48(1), 28; https://doi.org/10.3390/cimb48010028 - 25 Dec 2025
Cited by 1 | Viewed by 1005
Abstract
Background/Objectives: The enhancement of antitumor immune responses by radiotherapy (RT) is partially attributed to the activation of the IFN-type-I pathway. However, the loss of HLA-class-I molecules, which occurs in a large percentage of non-small-cell lung cancers (NSCLCs), may block the cytotoxic effect [...] Read more.
Background/Objectives: The enhancement of antitumor immune responses by radiotherapy (RT) is partially attributed to the activation of the IFN-type-I pathway. However, the loss of HLA-class-I molecules, which occurs in a large percentage of non-small-cell lung cancers (NSCLCs), may block the cytotoxic effect of T-cells and immunotherapy (IO). Moreover, autophagy is also involved in HLA downregulation. We investigated the complex interactions between RT, HLA molecules, autophagy, and IFN-type-I responses. Methods: The A549, H1299, and ATG7-deficient NSCLC cell lines, along with the modified shLC3A H1299 cell line, were used for in vitro experiments. The effect of RT (8 and 3 × 8 Gy) on Interferon beta (IFNβ), IFN-stimulated genes (ISGs), and HLA-class-I expression in combination with IFN-type-I-response inhibitors (Ruxolitinib, Tofacitinib, Amlexanox) targeting the JAK and TBK1 was studied with Flow cytometry and RT-PCR. Results: RT significantly induced HLA-class-I expression. A parallel upregulation of IFNβ and ISGs mRNA levels was also documented. Although the IFN-type-I-response inhibitors suppressed the RT-induced IFNβ and ISGs expression, their effect on HLA-class-I expression was minimal. Blockage of LC3A autophagy (shLC3A cell line) significantly upregulated HLA-class-I basal levels, and RT further enhanced HLA expression. IFN-type-I-response inhibitors blocked the RT-inductive effect in the shLC3A H1299, but had no effect in the ATG7-deficient H1650 cell line. Conclusions: The current study supports the theory that baseline autophagy, RT-induced autophagy blockage, and IFN-type-I response enhancement define the HLA-class-I levels in NSCLC cells. This complex interplay emerges as a promising target for the development of radio-vaccination strategies to enhance the efficacy of radio-immunotherapy. Full article
(This article belongs to the Special Issue Molecular Insights into Radiation Oncology)
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22 pages, 1830 KB  
Article
β-Arrestin 1 Differentially Modulates cAMP and ERK Pathways Downstream of the FSH Receptor
by Sei Hyun Park, Munkhzaya Byambaragchaa, Ye Rin Yu, Jae Won Lee, Min-Jeong Kwak, Seung-Bin Yoon, Ji-Su Kim, Myung-Hwa Kang and Kwan-Sik Min
Curr. Issues Mol. Biol. 2025, 47(12), 1051; https://doi.org/10.3390/cimb47121051 - 16 Dec 2025
Viewed by 783
Abstract
This study compared the gonadotropin gene sequences (LH and FSH subunits) of Cynomolgus and Rhesus monkeys and produced recombinant single-chain LHβ/α and FSHβ/α proteins. The α- and FSHβ-subunit sequences were identical between species, while LHβ showed only minor synonymous differences. The recombinant hormones [...] Read more.
This study compared the gonadotropin gene sequences (LH and FSH subunits) of Cynomolgus and Rhesus monkeys and produced recombinant single-chain LHβ/α and FSHβ/α proteins. The α- and FSHβ-subunit sequences were identical between species, while LHβ showed only minor synonymous differences. The recombinant hormones were successfully expressed and shown to be mainly N-glycosylated. Recombinant monkey FSHβ/α activated cAMP signaling in human FSH receptor-expressing cells, confirming its biological activity. β-arrestin 1 was found to have dual roles: its absence increased cAMP signaling (negative regulation), but it was required for ERK1/2 activation. ERK activation depended mainly on the cAMP/PKA pathway. Human and rat FSH receptors displayed different ERK activation timing, indicating species-specific signaling behavior. Overall, the study establishes a reliable system for producing functional recombinant monkey gonadotropins and clarifies how β-arrestin 1 differentially regulates FSH receptor signaling. Full article
(This article belongs to the Collection Advancements in Molecular Biology and Pharmaceutical Science)
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14 pages, 741 KB  
Review
Mitochondrial Dysfunction and Metabolic Reprogramming in Chronic Inflammatory Diseases: Molecular Insights and Therapeutic Opportunities
by Mi Eun Kim, Yeeun Lim and Jun Sik Lee
Curr. Issues Mol. Biol. 2025, 47(12), 1042; https://doi.org/10.3390/cimb47121042 - 14 Dec 2025
Cited by 22 | Viewed by 3725
Abstract
Chronic inflammatory diseases are driven by persistent immune activation and metabolic imbalance that disrupt tissue homeostasis. Mitochondrial dysfunction disrupts cellular bioenergetics and immune regulation, driving persistent inflammatory signaling. Mitochondrial dysfunction, characterized by excessive production of ROS, release of mitochondrial DNA, and defective mitophagy, [...] Read more.
Chronic inflammatory diseases are driven by persistent immune activation and metabolic imbalance that disrupt tissue homeostasis. Mitochondrial dysfunction disrupts cellular bioenergetics and immune regulation, driving persistent inflammatory signaling. Mitochondrial dysfunction, characterized by excessive production of ROS, release of mitochondrial DNA, and defective mitophagy, amplifies inflammatory signaling and contributes to disease progression. Meanwhile, metabolic reprogramming in immune and stromal cells establishes distinct bioenergetic profiles. These profiles maintain either pro-inflammatory or anti-inflammatory phenotypes through key signaling regulators such as HIF-1α, AMPK, mTOR, and SIRT3. Crosstalk between mitochondrial and metabolic pathways determines whether inflammation persists or resolves. Recent advances have identified critical molecular regulators, including the NRF2–KEAP1 antioxidant system, the cGAS–STING innate immune pathway, and the PINK1–Parkin mitophagy pathway, as potential therapeutic targets. Pharmacologic modulation of metabolic checkpoints and restoration of mitochondrial homeostasis represent key strategies for re-establishing cellular homeostasis. Developing approaches, including NAD+ supplementation, mitochondrial transplantation, and gene-based interventions, also show significant therapeutic potential. This review provides a mechanistic synthesis of how mitochondrial dysfunction and metabolic reprogramming cooperate to maintain chronic inflammation and highlights molecular pathways that represent promising targets for precision therapeutics in inflammatory diseases. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Innovative Therapeutic Approaches in Inflammatory Diseases, Pioneering Precision Medicine Solutions)
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14 pages, 2214 KB  
Article
Evaluation of the Role of AID-Induced Mutagenesis in Resistance to B-Cell Receptor Pathway Inhibitors in Chronic Lymphocytic Leukemia
by Chiara Pighi, Alessandro Gasparetto, Elisa Genuardi, Jianli Tao, Qi Wang, Candida Vitale, Valentina Griggio, Rocco Piazza, Sabino Ciavarella, Marta Coscia, Simone Ferrero, Alberto Zamò, Claudia Voena and Roberto Chiarle
Curr. Issues Mol. Biol. 2025, 47(12), 1031; https://doi.org/10.3390/cimb47121031 - 10 Dec 2025
Viewed by 1020
Abstract
Chronic lymphocytic leukemia (CLL) is the most common leukemia in Western countries, and B-cell receptor (BCR) pathway inhibitors such as idelalisib and ibrutinib are currently established therapies for CLL. Although effective, these drugs frequently lead to resistance, but the mechanisms are still not [...] Read more.
Chronic lymphocytic leukemia (CLL) is the most common leukemia in Western countries, and B-cell receptor (BCR) pathway inhibitors such as idelalisib and ibrutinib are currently established therapies for CLL. Although effective, these drugs frequently lead to resistance, but the mechanisms are still not fully understood. Activation-induced cytidine deaminase (AID) is a B-cell enzyme essential for antibody diversification. However, it can also introduce off-target mutations, leading to genomic instability. This study investigates whether treatment with BCR pathway inhibitors increases AID activity in CLL and whether this activity contributes to the development of drug resistance. Peripheral blood samples from CLL patients were collected before and after treatment with idelalisib or ibrutinib. Targeted sequencing was used to identify mutations in known AID off-target genes. Concurrently, AID-wild type (AID-WT) and AID-knockout (AID-KO) CLL cell lines were established and subsequently exposed to escalating doses of BCR pathway inhibitors to develop drug-resistant models. In patient samples, treatment with BCR pathway inhibitors was associated with an increase in AID-dependent mutations in off-target genes, including BCL2, MYC, and IRF8. The in vitro models efficiently recapitulated the patients’ data, as only AID-WT CLL cells accumulated mutations in the same AID off-target genes after drug exposure. However, no mutations were detected in genes that could mediate drug resistance. We conclude that BCR pathway inhibitors enhance AID mutational activity in CLL, but this does not appear to be directly involved in driving drug resistance. AID-targeted loci may nonetheless serve as biomarkers for monitoring genomic instability during treatment and inform further study. Full article
(This article belongs to the Section Molecular Medicine)
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