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Cells

Cells is an international, peer-reviewed, open access journal on cell biology, molecular biology, and biophysics, published semimonthly online by MDPI. The Nordic Autophagy Society (NAS), the Spanish Society of Hematology and Hemotherapy (SEHH), the International Cell Death Society (ICDS), the Spanish Group for Hematopoietic Transplantation and Cell Therapy (GETH-TC), and the Epigenetics Society (ES) are affiliated with Cells, and their members receive discounts on the article processing charges.

Open Access— free for readers, with article processing charges (APC) paid by authors or their institutions.
High Visibility: indexed within Scopus, SCIE (Web of Science), PubMed, MEDLINE, PMC, CAPlus / SciFinder, and other databases.
Journal Rank: JCR - Q2 (Cell Biology) / CiteScore - Q1 (General Biochemistry, Genetics and Molecular Biology)
Rapid Publication: manuscripts are peer-reviewed and a first decision is provided to authors approximately 14.9 days after submission; acceptance to publication is undertaken in 2.8 days (median values for papers published in this journal in the first half of 2026).
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 21 topical sections.
Companion journal: Organoids.

Impact Factor: 6.0 (2025); 5-Year Impact Factor: 6.6 (2025)

Imprint Information Journal Flyer Open Access ISSN: 2073-4409

Latest Articles

25 pages, 3795 KB

Open AccessArticle

AI-Assisted Multimodal Transcriptomic Analysis Identifies a Senescence-Related Prognostic Signature and Characterizes ADGRF5-Associated Malignant Phenotypes in Breast Cancer

by Wenhao Liu, Wenhui Wu, Shubai Chen, Kaiqiong Chen and Xin Li

Cells 2026, 15(17), 1589; https://doi.org/10.3390/cells15171589 (registering DOI) - 1 Sep 2026

Cellular senescence (CS) is increasingly recognized as an important cell-state programme involved in breast cancer progression and therapeutic response, but its context-dependent molecular heterogeneity limits its application in prognostic assessment. In this study, GeneCompass-based all-gene in silico perturbation analysis was performed to identify [...] Read more.

Cellular senescence (CS) is increasingly recognized as an important cell-state programme involved in breast cancer progression and therapeutic response, but its context-dependent molecular heterogeneity limits its application in prognostic assessment. In this study, GeneCompass-based all-gene in silico perturbation analysis was performed to identify candidate genes predicted to induce senescence or rejuvenation, thereby expanding the known senescence-related gene set. Machine learning further established a seven-gene prognostic signature that may serve as an adjunctive tool for prognostic assessment across multiple cohorts. The time-dependent AUCs at 1, 3, and 5 years were 0.707, 0.700, and 0.684 in the training cohort; 0.657, 0.661, and 0.629 in the test cohort; and 0.611, 0.646, and 0.637 in the external validation cohort, respectively. Single-cell and spatial transcriptomic analyses suggested that the risk component of the prognostic signature reflects not only malignant epithelial cell states but also stromal–vascular remodelling in the tumor microenvironment. Among the signature genes, ADGRF5 exhibited the most pronounced expression alteration, and its knockdown suppressed malignant phenotypes in breast cancer cells. These findings provide an AI-assisted strategy for senescence biomarker discovery and highlight ADGRF5 as a candidate functional risk gene associated with breast cancer progression. Full article

(This article belongs to the Special Issue Molecular Biomarkers in Tumors: Prognosis and Mechanisms)

31 pages, 5776 KB

Open AccessReview

Molecular Pathways, Target Landscape, and Translational Models in Heart Failure with Preserved Ejection Fraction

by Haleema Qamar, Janmeet S. Saini, Sylwia Marta Figarska, Emmanuel S. Buys and Vilas Wagh

Cells 2026, 15(17), 1588; https://doi.org/10.3390/cells15171588 - 1 Sep 2026

Heart failure with preserved ejection fraction (HFpEF) is a substantial global health burden and the greatest unmet medical need for cardiovascular diseases. It is marked by pronounced clinical heterogeneity and complex multi-system pathophysiology with limited therapeutic options. Progress in developing effective therapeutics is [...] Read more.

Heart failure with preserved ejection fraction (HFpEF) is a substantial global health burden and the greatest unmet medical need for cardiovascular diseases. It is marked by pronounced clinical heterogeneity and complex multi-system pathophysiology with limited therapeutic options. Progress in developing effective therapeutics is constrained by the inadequacy of experimental models to fully recapitulate the multifactorial nature of the disease. Recent evidence underscores the significant involvement of inflammatory, oxidative, and mitochondrial pathways in the pathogenesis of HFpEF, with non-coding RNAs and epigenetic regulation serving as crucial modulators and prospective therapeutic targets. This review maps the HFpEF target landscape, while critically assessing the mechanistic contributions, translational fidelity, and limitations of existing in vivo and in vitro models. Further, advances are noted among the in vitro technologies, including human cardiac organoids and engineered heart tissues integrated with high-throughput multi-omics and computational modeling, enabling in-depth examination of HFpEF mechanisms. Finally, we underscore the necessity of integrative, systems-level approaches and multi-marker strategies to enhance translational relevance, improve risk stratification, and accelerate development of mechanism-based therapies. Collectively, this review supports phenotypic-guided and mechanism-informed therapeutic development for HFpEF, and provides a roadmap for next generation model development and therapeutic innovation. Full article

(This article belongs to the Special Issue Advances in Cardiometabolic Pathophysiology and Treatment)

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3 pages, 156 KB

Open AccessEditorial

Advances in the Cellular and Molecular Mechanisms of Cardiovascular Diseases

by Katie S. Wraith and Timothy M. Palmer

Cells 2026, 15(17), 1587; https://doi.org/10.3390/cells15171587 - 1 Sep 2026

Cardiovascular diseases (CVDs) remain the leading cause of death worldwide despite major advances in prevention, diagnosis and treatment [...] Full article

(This article belongs to the Special Issue Advances in the Cellular and Molecular Mechanisms of Cardiovascular Diseases)

18 pages, 30786 KB

Open AccessArticle

Age-Associated YBX1 Phosphorylation Regulates the Keratinocyte Senescence-Associated Secretory Phenotype Through Translational Control

by Valdi Ven Japranata, Michelle Liu, Fabiana Boncimino, Emery Di Cicco, Sara Palumbo, Kristina Todorova, Enkhtuul Gantumur, Stefano Sol and Anna Mandinova

Cells 2026, 15(17), 1586; https://doi.org/10.3390/cells15171586 - 1 Sep 2026

Skin aging is characterized by epidermal atrophy, reduced keratinocyte proliferation, and the accumulation of senescent cells that sustain a chronic, low-grade inflammatory secretome known as the senescence-associated secretory phenotype (SASP). We previously showed that Y-box binding protein 1 (YBX1) limits keratinocyte senescence in [...] Read more.

Skin aging is characterized by epidermal atrophy, reduced keratinocyte proliferation, and the accumulation of senescent cells that sustain a chronic, low-grade inflammatory secretome known as the senescence-associated secretory phenotype (SASP). We previously showed that Y-box binding protein 1 (YBX1) limits keratinocyte senescence in human epidermis by acting as a translational repressor of SASP chemokines, including CXCL1 and IL8. How this brake is regulated during skin aging, however, remains undefined. Here we demonstrate that, although total YBX1 protein is reduced in keratinocytes from aged human epidermis, the fraction of phosphorylated YBX1 (pYBX1) is increased relative to young donors, resulting in an elevated pYBX1/total YBX1 ratio that correlates with chronological age. Because pYBX1 is predominantly nuclear, whereas unphosphorylated YBX1 is cytoplasmic, this shift is predicted to deplete the cytoplasmic pool available for translational repression of CXCL1 and IL8. Consistent with this model, treatment of immortalized (Ker-CT) and primary human keratinocytes (HK) with the PI3K inhibitors PI-103 and GDC-0941 suppressed YBX1 phosphorylation without altering total YBX1 abundance, thus retaining YBX1 in the cytoplasm. This allows cytoplasmic YBX1 to re-engage and repress the translation of CXCL1 and IL8 mRNAs, lower chemokine secretion, and reduce the fraction of senescent keratinocytes. Moreover, conditioned medium from PI-103- or GDC-0941-treated cells sufficiently decreased senescence in recipient cells, consistent with a paracrine, secretome-mediated effect. Together, these findings support an association between YBX1 phosphorylation and SASP chemokine output in aging human keratinocytes and nominate YBX1-directed modulation as a candidate strategy for selectively attenuating senescence-associated secretory phenotypes in intrinsic skin aging. Full article

(This article belongs to the Special Issue Molecular Mechanisms of Programmed Cell Death in Disease Pathogenesis and Targets for Therapeutic Intervention)

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16 pages, 885 KB

Open AccessArticle

Therapeutic Potential of Intra-Articular Delivery of Allogeneic Dedifferentiated Fat Cells in a Canine Monoiodoacetate-Induced Knee Osteoarthritis Model

by Rei Nakano, Azusa Seki and Hiroshi Sugiya

Cells 2026, 15(17), 1585; https://doi.org/10.3390/cells15171585 - 31 Aug 2026

Osteoarthritis (OA) is the leading cause of disability worldwide. Although rodent models are widely used in OA research, the disease is often artificially accelerated in these systems, and joint biomechanics differ substantially from those of humans. In contrast, canine models offer greater translational [...] Read more.

Osteoarthritis (OA) is the leading cause of disability worldwide. Although rodent models are widely used in OA research, the disease is often artificially accelerated in these systems, and joint biomechanics differ substantially from those of humans. In contrast, canine models offer greater translational relevance due to similarities in joint size, cartilage thickness, and physiological mechanical loading of the knee, making them suitable surrogates for evaluating regenerative therapies. In this study, we assessed the therapeutic efficacy of allogeneic dedifferentiated fat (DFAT) cells, which exhibit greater cellular homogeneity and enhanced osteochondrogenic potential compared with conventional mesenchymal stem cells (MSCs), in a canine monoiodoacetate (MIA)-induced OA model. OA was induced by intra-articular (i.a.) injection of MIA into the knee joints of beagles. Animals were allocated to three groups: an implant group receiving allogeneic DFAT cells via i.a. injection, a vehicle group, and a sham group. Therapeutic outcomes were evaluated through macroscopic scoring of cartilage surfaces and histological assessment using toluidine blue staining to examine proteoglycan depletion and structural integrity. The implant group demonstrated significantly lower Osteoarthritis Research Society International (OARSI) scores for cartilage erosion and osteophyte formation compared with the vehicle group, indicating preservation of joint surface integrity. Toluidine blue staining further showed that DFAT cell implantation significantly preserved extracellular matrix components, with greater proteoglycan retention relative to vehicle-treated controls. A key rationale for employing a canine model was the high prevalence of spontaneous OA in dogs, which closely resembles human disease in clinical presentation, radiographic findings, and molecular pathways. Unlike rodent models, dogs naturally develop OA with progressive degenerative features that mirror human conditions. By utilizing a large animal model, this study bridges the gap between preclinical in vitro findings and potential human clinical application. Collectively, these results provide strong evidence supporting the therapeutic potential of allogeneic DFAT cells and suggest that DFAT-based therapy may represent a promising treatment strategy for chronic, naturally occurring OA in both veterinary and human patients. Full article

(This article belongs to the Topic Animal Models of Human Disease 3.0)

22 pages, 1326 KB

Open AccessArticle

Beta Cell Proinsulin Response to Amino Acid Availability

by Yuting Ruan, Noah F. Gleason and Peter Arvan

Cells 2026, 15(17), 1584; https://doi.org/10.3390/cells15171584 - 31 Aug 2026

Through fasting and feeding (both in vivo and in vitro), nutrient availability fluctuates over time. Pancreatic β-cells must respond to nutrients not only by regulated insulin secretion but also by insulin synthesis, which depends upon proinsulin. β-cells respond biosynthetically to glucose, but little [...] Read more.

Through fasting and feeding (both in vivo and in vitro), nutrient availability fluctuates over time. Pancreatic β-cells must respond to nutrients not only by regulated insulin secretion but also by insulin synthesis, which depends upon proinsulin. β-cells respond biosynthetically to glucose, but little is known about amino acids as regulators of proinsulin levels. We find that in INS1E (rat) β-cells, isolated murine islets, and isolated human islets—even in the presence of abundant glucose, proinsulin levels remain sensitive to reduced availability of other nutrients contained in β-cell/islet bathing medium. A low proinsulin level upon in vitro fasting is accompanied by diminished ribosomal phospho-S6 and phospho-eIF4E-BP1 plus increased phospho-eIF2α, reversed upon re-feeding. Even as extracellular glucose levels remained steady, INS1E cells consumed the majority of extracellular glutamine and serine (measured by mass spectrometry); concurrently, six nonessential amino acids (most notably proline and alanine, plus glutamic and aspartic acid) were actually exported from cells to media. Proinsulin suppression in response to amino acid limitation appears to be β-cell-autonomous, is linked to proinsulin biosynthesis, and is ameliorated upon GCN2 inhibition in INS1E cells. Upon re-feeding amino acid-containing medium, the mTORC1 inhibitor rapamycin fully suppressed phospho-S6 but did not block the recovery of proinsulin levels, whereas Torin1 inhibition of mTOR inhibited the amino acid-dependent increase in proinsulin biosynthesis. Altogether, these data indicate that inadequate amino acid-triggered β-cell signaling can blunt the proinsulin biosynthetic response, contributing to insulin deficiency—a finding that has potential relevance to the pathogenesis of malnutrition-related diabetes. Full article

(This article belongs to the Special Issue Cellular Signalling Pathways in the Endocrine Pancreas and Diabetes)

35 pages, 2438 KB

Open AccessArticle

The Making of Synaptic Ribbons: Carboxy-Terminal Tagging of RIBEYE B-Domain Reduces Steady-State Levels of RIBEYE and Its Efficacy to Build Synaptic Ribbons

by Ajay Kesharwani, Marie-Lisa Eich, Amrita Mukherjee, Stephan Maxeiner, Gabriele Kiefer, Gabriela Krasteva-Christ, Karin Schwarz and Frank Schmitz

Cells 2026, 15(17), 1583; https://doi.org/10.3390/cells15171583 - 31 Aug 2026

RIBEYE is the central building block of synaptic ribbons, the eponymous presynaptic specializations of ribbon synapses. RIBEYE consists of two major protein regions: a unique amino-terminal, proline-rich A-domain and a carboxy-terminal, NADH-binding B-domain, which is largely identical to tetramer-forming nuclear protein CtBP2. In [...] Read more.

RIBEYE is the central building block of synaptic ribbons, the eponymous presynaptic specializations of ribbon synapses. RIBEYE consists of two major protein regions: a unique amino-terminal, proline-rich A-domain and a carboxy-terminal, NADH-binding B-domain, which is largely identical to tetramer-forming nuclear protein CtBP2. In RIBEYE knockout mice, synaptic ribbons are completely absent, emphasizing the central role of RIBEYE in making synaptic ribbons. In the present study, we used a previously generated transgenic RIBEYE mouse line, in which a large protein tag was fused to the carboxy-terminus of RIBEYE-B-domain (RIBEYE-C-TG). We generated RIBEYE-C-TG-expressing RIBEYE knockout mice to study the impact of carboxy-terminal tagging of RIBEYE B-domain on synaptic ribbon formation. We applied high-resolution confocal immunofluorescence microscopy, conventional and E-PTA transmission electron microscopy to analyze whether carboxy-terminally tagged RIBEYE-C-TG rescues synaptic ribbon deficiency in RIBEYE knockout mice and restores synaptic ribbon in situ. High-resolution immunofluorescence microscopy revealed that transgenic RIBEYE-C-TG expression rescued synaptic ribbon formation in RIBEYE knockout mice. Electron microscopy confirmed that transgenic ribbons consisting of transgenic RIBEYE-C-TG were made, anchored to the active zone, and associated with synaptic vesicles. But transgenic synaptic ribbons formed by RIBEYE-C-TG were considerably smaller in size than synaptic ribbons in control mice. The expression level of RIBEYE-C-TG protein was much lower than untagged RIBEYE protein as demonstrated by qualitative and quantitative Western blot analyses. The decreased expression level of RIBEYE-C-TG protein is not due to decreased activity of the transgenic RIBEYE promoter or alterations of the 5′-UTR as shown by RT-qPCR analyses of RIBEYE transcripts and reporter assays. Our findings suggest that carboxy-terminally tagged RIBEYE-C-TG protein is less stable and less efficient in making synaptic ribbons than the untagged RIBEYE protein. Based on the findings in this study and on recently published structural data from other groups on RIBEYE and RIBEYE B-domain/CtBP2, we predict that carboxy-terminal tagging of RIBEYE B-domain, placed at the interaction interface of RIBEYE B-domain tetramers/RIBEYE B-domain filaments, could interfere with the formation and/or stability of RIBEYE B-domain-dependent oligomeric complexes which are likely essential to build the synaptic ribbon. Full article

(This article belongs to the Special Issue Molecular Anatomy and Function of Sensory Organs and Sensory Tissues)

18 pages, 1020 KB

Open AccessArticle

WNK1 Phosphorylation Sites in TBC1D1 and TBC1D4 Modulate Cell-Surface Abundance of GLUT1

by Andreia F. A. Henriques, Paulo Matos, Ana Sofia Carvalho, Mikel Azkargorta, Felix Elortza, Rune Matthiesen and Peter Jordan

Cells 2026, 15(17), 1582; https://doi.org/10.3390/cells15171582 - 31 Aug 2026

This manuscript is the corrected version of a previously published paper. Glucose uptake by mammalian cells is a key mechanism to maintain cell and tissue homeostasis and relies mostly on plasma membrane-localized glucose transporter proteins (GLUTs). Two main cellular mechanisms regulate GLUT proteins [...] Read more.

This manuscript is the corrected version of a previously published paper. Glucose uptake by mammalian cells is a key mechanism to maintain cell and tissue homeostasis and relies mostly on plasma membrane-localized glucose transporter proteins (GLUTs). Two main cellular mechanisms regulate GLUT proteins in the cell: first, expression of GLUT genes is under dynamic transcriptional control and is used by cancer cells to increase glucose availability. Second, GLUT proteins are regulated by membrane traffic from storage vesicles to the plasma membrane (PM). This latter process is triggered by signaling mechanisms and is well studied in the case of insulin-responsive cells, which activate protein kinase AKT to phosphorylate TBC1D4, a RAB-GTPase–activating protein involved in membrane traffic regulation. Previously, we identified protein kinase WNK1 as another kinase able to phosphorylate TBC1D4 and regulate the surface abundance of the constitutive glucose transporter GLUT1. Here we describe that downregulation of WNK1 through RNA interference in HEK293 cells led to a two-fold decrease in cell-surface GLUT1 abundance, concomitant with a 40% decrease in glucose uptake. By mass spectrometry, we identified serine (S) 704 in TBC1D4 and also S565 in its paralogue TBC1D1 as candidate WNK1 phosphorylation sites. Transfection of the respective phosphomimetic or unphosphorylatable TBC1D mutants into cells revealed that both affected the cell-surface abundance of GLUT1. The results reinforce a regulatory role for WNK1 in GLUT1 trafficking and glucose uptake and may have potential impact for the understanding of metabolic dysregulation, as observed in many cancer cells or insulin-responsive cell types. Full article

(This article belongs to the Section Cell Signaling)

31 pages, 5008 KB

Open AccessArticle

Use of Neuronal-Enriched Extracellular Vesicles to Distinguish Cognitive Impairment Levels and Sex Differences in People with HIV

by Norina Tang, Fan Xia, Heather Freasier, Phyllis C. Tien, Marshall J. Glesby, Daniel Merenstein, Audrey L. French, Heather McKay, Monica M. Diaz, Igho Ofotokun, Jordan E. Lake, Joseph B. Margolick, Eun-Young Kim, Steven R. Levine, Margaret A. Fischl, Wei Li, Jeremy Martinson and Lynn Pulliam

Cells 2026, 15(17), 1581; https://doi.org/10.3390/cells15171581 - 31 Aug 2026

Cognitive impairment still occurs despite well-controlled HIV but with milder symptoms. People with and without HIV have different neuronal protein changes that may differentiate the asymptomatic neurocognitive impairment (ANI) condition from normal cognition (NPN) and mild neurocognitive disorder (MND). Plasma neuronal-enriched extracellular vesicles [...] Read more.

Cognitive impairment still occurs despite well-controlled HIV but with milder symptoms. People with and without HIV have different neuronal protein changes that may differentiate the asymptomatic neurocognitive impairment (ANI) condition from normal cognition (NPN) and mild neurocognitive disorder (MND). Plasma neuronal-enriched extracellular vesicles (nEVs) were isolated from people with HIV (PWH) with NPN, ANI, or MND, and HIV seronegative controls with NPN (HIV−). Two different platforms were used to delineate protein patterns between sexes and cognitive conditions. When combining results from men and women, the nEV cargo in many cases showed little difference between cognitive conditions. However, when separated, there were different patterns between the sexes for some nEV cargo that distinguished the HIV− groups and HIV+ cognition groups. PWH with NPN had higher nEV toxic proteins compared to individuals without HIV. Women with HIV showed perfect separation between NPN and ANI with Aβ42 and NCAM-1 and perfect separation between ANI and MND with Aβ40 and NCAM-1. Men with HIV with MND had significantly higher NCAM-1 when compared to ANI, and lower GLRX when compared to NPN. This study shows distinct markers for different HIV cognitive categories, many of which differed between men and women. Full article

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27 pages, 6324 KB

Open AccessArticle

Comprehensive Phenotyping of Circulating T- and B-Cell Subsets in Patients with Ankylosing Spondylitis Associated with Crohn’s Disease

by Artem Rubinstein, Arthur Aquino, Denis Davydov, Oksana Shchukina, Zoia Korobova, Jennet Mammedova, Eleonora Starikova, Valerii Marchenko, Michael Galagudza and Igor Kudryavtsev

Cells 2026, 15(17), 1580; https://doi.org/10.3390/cells15171580 - 31 Aug 2026

Background: Ankylosing spondylitis (AS) associated with Crohn’s disease (CD) is a nosological form of spondyloarthropathies with a low population prevalence. The pathogenesis of this disease is not fully understood, and there are no precise differential diagnostic methods to distinguish AS associated with CD [...] Read more.

Background: Ankylosing spondylitis (AS) associated with Crohn’s disease (CD) is a nosological form of spondyloarthropathies with a low population prevalence. The pathogenesis of this disease is not fully understood, and there are no precise differential diagnostic methods to distinguish AS associated with CD from AS and CD separately in the early stages of the disease. The main objective for this study is to define lymphocyte-mediated immunity in patients with AS associated with CD. Methods: For the pilot study, we recruited four groups: CD (n = 16), AS+CD (n = 13), AS (n = 13) and healthy controls (HC, n = 26). Immune phenotyping of peripheral blood lymphocytes was carried out via flow cytometry. Results: In the AS+CD group, circulating regulatory T-cell (Treg) levels were increased compared to the other groups. The frequency of CD73+ Tregs within the effector memory (EM) compartment was also elevated in the AS+CD group relative to the AS and CD groups alone. At the same time, the EM Tcyt and EM Th populations were lower in the AS+CD group compared to the CD group. Tfh17 levels were lower in the AS+CD group than in the AS group and showed a positive correlation with Bm5 and ‘switched’ memory B cells. Additionally, Tfh17 and ‘switched’ memory B cells correlated negatively with acute-phase markers, whereas Tfh2 correlated positively with the BASDAI activity index. Conclusions: In patients with AS associated with CD, exhaustion of the regulatory compartment of adaptive immunity is seen, whereas the humoral component appears oriented towards resolving the inflammatory responses. Full article

(This article belongs to the Special Issue Autoimmune Diseases: Immune Cells and Genetic and Epigenetic Regulations)

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20 pages, 1931 KB

Open AccessArticle

Blood Eosinophil Subtype-Specific Protein Gene Expression and Eosinophil-Derived Serum Mediators in Allergic Asthma Patients After Bronchial Challenge with Dermatophagoides pteronyssinus

by Airidas Rimkunas, Andrius Januskevicius, Egle Vasyle, Jolita Palacionyte, Skaidrius Miliauskas and Kestutis Malakauskas

Cells 2026, 15(17), 1579; https://doi.org/10.3390/cells15171579 - 30 Aug 2026

Background: Differences in gene expression between inflammatory-like (iEOS-like) and resident-like (rEOS-like) eosinophil subtypes, and in eosinophil-derived serum mediators, may reflect eosinophil functional activity and their potential role in the pathogenesis of allergic asthma (AA). Methods: Twenty-three patients with non-severe AA and thirteen healthy [...] Read more.

Background: Differences in gene expression between inflammatory-like (iEOS-like) and resident-like (rEOS-like) eosinophil subtypes, and in eosinophil-derived serum mediators, may reflect eosinophil functional activity and their potential role in the pathogenesis of allergic asthma (AA). Methods: Twenty-three patients with non-severe AA and thirteen healthy subjects (HS) were examined. AA patients underwent a bronchial allergen challenge (BAC) with Dermatophagoides pteronyssinus and were re-evaluated 24 h later. Blood eosinophils were isolated by gradient centrifugation and magnetic separation, followed by subtyping based on CD62L expression. Gene expression was assessed by TaqMan-based quantitative PCR. Serum eosinophil cationic protein (ECP), eosinophil-derived neurotoxin (EDN), Galectin-10 (Gal10), and NADPH oxidase 2 (NOX2) were measured using ELISA. Results: Blood eosinophil subtypes from AA patients showed significantly higher expression of CLC, ECP, EPX, EDN, MBP, ALOX5, NOX2, and TGF-β1 compared to those from HS (p < 0.05), with no significant changes in LTA4H and LTC4S. iEOS-like cells in AA patients exhibited higher CLC and EPX expression compared to rEOS-like cells, (p < 0.05). Following BAC, CLC, MBP, and TGF-β1 expression increased in both eosinophil subtypes, while EPX and NOX2 increased only in iEOS-like cells (all p < 0.05). Serum ECP, EDN, and Gal10 concentrations were elevated in AA compared to HS and further increased after BAC (all p < 0.05); serum NOX2 remained unchanged. Conclusions: BAC induces a late-phase eosinophilic response in AA characterized by a partially eosinophil subtype-specific increase in gene expression and in circulating eosinophil-derived mediators. An increase in Gal10, observed at the CLC transcript level in eosinophils and in serum—but not in ECP or EDN—suggests the existence of mediator-specific mechanisms that regulate gene expression and extracellular release. Full article

(This article belongs to the Special Issue Recent Advances in Immunology of Asthma)

15 pages, 696 KB

Open AccessReview

Beyond Weight Loss: Thromboinflammation as a Candidate Mechanism for the Cardiovascular Benefit of GLP-1 Receptor Agonists

by Ivan Melnikov, Daria Borodko and Vyacheslav Alekseev

Cells 2026, 15(17), 1578; https://doi.org/10.3390/cells15171578 - 30 Aug 2026

Glucagon-like peptide-1 receptor agonists (GLP-1RAs) have emerged as an important class of medications for managing type 2 diabetes and obesity, with cardiovascular outcome trials demonstrating reductions in major adverse cardiovascular events (MACEs) for several agents. The SELECT trial, which enrolled 17,604 participants with [...] Read more.

Glucagon-like peptide-1 receptor agonists (GLP-1RAs) have emerged as an important class of medications for managing type 2 diabetes and obesity, with cardiovascular outcome trials demonstrating reductions in major adverse cardiovascular events (MACEs) for several agents. The SELECT trial, which enrolled 17,604 participants with established cardiovascular disease and overweight or obesity but without diabetes, showed a 20% reduction in MACEs with semaglutide compared with placebo. Importantly, mediation analyses indicated that weight loss accounted for approximately one-third of this cardiovascular benefit, suggesting that additional mechanisms contribute substantially to the observed risk reduction. The temporal dissociation between weight loss and early MACEs reduction supports the hypothesis that GLP-1RAs exert direct vascular protective effects independent of their metabolic actions. This review synthesizes current evidence on the thromboinflammatory mechanisms through which GLP-1RAs may exert their cardiovascular benefits, with particular emphasis on the neutrophil–NET axis, platelet function, and plaque stabilization. Overall, thromboinflammation represents a biologically reasonable candidate mechanism, but its contribution to the cardiovascular benefit of GLP-1RAs treatment is an open question. Still, residual treatment effects cannot be attributed specifically to thromboinflammation, because metabolic, renal, hemodynamic, and vascular pathways, among others, may also contribute. Full article

29 pages, 8119 KB

Open AccessArticle

MBD3 Knockdown Promotes the Differentiation of Bovine iPSCs into Primordial Germ Cell-like Cells Associated with Altered Bivalent Modification of TGF-β-Related Genes

by Wen Yuan, Jing Wang, Weiqi Li, Yang Luo, Yiting Liu, Shun Long, Yiyang Wang, Fang Liu, Xiaoxiong Geng, Yongli Yue and Xueling Li

Cells 2026, 15(17), 1577; https://doi.org/10.3390/cells15171577 - 30 Aug 2026

Methyl-CpG binding domain protein 3 (MBD3) is a member of the nucleosome remodeling and deacetylase (NuRD) corepressor protein complex, which plays a pivotal role in embryonic development, pluripotent stem cell (PSC) differentiation, and induced pluripotent stem cell (iPSC) reprogramming. However, whether MBD3 is [...] Read more.

Methyl-CpG binding domain protein 3 (MBD3) is a member of the nucleosome remodeling and deacetylase (NuRD) corepressor protein complex, which plays a pivotal role in embryonic development, pluripotent stem cell (PSC) differentiation, and induced pluripotent stem cell (iPSC) reprogramming. However, whether MBD3 is also involved in iPSC differentiation into primordial germ cell-like cells (PGCLCs) is unclear. In this study, bovine iPSCs generated by MBD3 knockdown (MBD3 KD) during reprogramming were subjected to PGCLC differentiation using a monolayer cell culture method. Our results revealed that MBD3 KD enhanced the ability of bovine iPSCs to differentiate into PGCLCs. MBD3-KD bovine iPSC-derived PGCLCs exhibited the characteristics of in vivo primordial germ cells (PGCs) in a migratory state. MBD3 KD increased NODAL signal transduction during the induction of PGCLCs and was associated with increased expression of PRDM1 and SOX15. Moreover, MBD3 KD increased the bivalent modification of transforming growth factor beta (TGF-β)-related genes concomitant with the upregulation of DPPA4 and DNMT3L expression in bovine iPSCs, and this epigenetic change was associated with enhanced NODAL signaling. Our results indicate that MBD3 KD during reprogramming favors the differentiation of bovine iPSCs into PGCLCs, further highlighting the impact of MBD3 on histone modifications during germ cell development. Full article

(This article belongs to the Section Cell Signaling)

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20 pages, 331 KB

Open AccessReview

Immune Dysregulation, Compartment-Specific Biology, and Therapeutic Biomarkers in Mycosis Fungoides and Sézary Syndrome

by Tiantian Zhang, Weili Xue, Simo Du, Jiahe Zhao and Yumeng Zhang

Cells 2026, 15(17), 1576; https://doi.org/10.3390/cells15171576 - 30 Aug 2026

Cutaneous T-cell lymphoma (CTCL), including mycosis fungoides (MF) and Sézary syndrome (SS), is defined by malignant CD4+ T-cell clones that evolve within and remodel the skin and systemic immune compartments. For disease biology and immune remodeling, we prioritize evidence from human primary samples; [...] Read more.

Cutaneous T-cell lymphoma (CTCL), including mycosis fungoides (MF) and Sézary syndrome (SS), is defined by malignant CD4+ T-cell clones that evolve within and remodel the skin and systemic immune compartments. For disease biology and immune remodeling, we prioritize evidence from human primary samples; for therapeutic implications, we integrate clinical-trial and translational biomarker studies. We organize evidence by compartment (skin vs. blood) and, within skin, by stage (patch/plaque vs. tumor). Early patch/plaque MF often shows features consistent with constrained inflammation: skin-resident memory T-cell (TRM)-like malignant clones are in a Th1-leaning microenvironment with relatively preserved cytotoxic surveillance. Progression to tumor-stage MF (and/or large-cell transformation) is frequently associated with clonal dominance, Th2 cytokine polarization, upregulation of checkpoint pathways, and remodeling of myeloid/fibroblast populations. SS is typically associated with leukemic clonal dominance, systemic Th2 skewing, and broad impairment of cytotoxic immune control. These trajectories support an interpretive framework that aligns immune-directed therapies with compartment- and stage-associated biology; these include strategies that (i) deplete malignant clones (e.g., CCR4, CD30, KIR3DL2 targeting), (ii) re-engage exhausted effectors (PD-1/PD-L1 axis), (iii) reprogram cytokine balance (IFN-γ, IL-12, extracorporeal photopheresis), or (iv) suppress malignant signaling programs with secondary immune effects (JAK/STAT inhibition). We highlight potential candidate predictive biomarkers at varying levels of maturity, most of which require prospective validation, including antigen density, compartmental tumor burden, tumor cell fraction, effector-cell substrate, and interferon/cytokine signatures. Full article

(This article belongs to the Special Issue Advances in the Biology and Treatment of T-Cell Lymphoma)

43 pages, 4790 KB

Open AccessReview

Emerging Nucleic Acid-Based Therapies for Hypercholesterolemia with Focus on a New Modality, Liver-Directed miR-30c Analog C2

by Rai Ajit K. Srivastava

Cells 2026, 15(17), 1575; https://doi.org/10.3390/cells15171575 - 29 Aug 2026

Despite major advances in lipid-lowering therapies, a significant unmet need remains, particularly for patients with homozygous familial hypercholesterolemia (HoFH), severe heterozygous familial hypercholesterolemia (HeFH), and those who fail to achieve guideline-recommended LDL-C targets. Nucleic acid-based therapeutics have emerged as a transformative approach for [...] Read more.

Despite major advances in lipid-lowering therapies, a significant unmet need remains, particularly for patients with homozygous familial hypercholesterolemia (HoFH), severe heterozygous familial hypercholesterolemia (HeFH), and those who fail to achieve guideline-recommended LDL-C targets. Nucleic acid-based therapeutics have emerged as a transformative approach for treating hypercholesterolemia. Antisense oligonucleotides and small interfering RNAs (siRNAs) have demonstrated durable hepatic gene silencing and have led to approved therapies, while gene replacement and in vivo genome-editing strategies offer the potential for long-lasting, and possibly one-time, interventions. In parallel, microRNAs (miRNAs) have attracted increasing interest because of their ability to coordinately regulate multiple genes involved in lipoprotein metabolism, cholesterol transport, and lipid homeostasis. Human genetic studies further support the importance of miRNA-mediated regulation, exemplified by a rare ~2.5 kb deletion in the distal LDLR 3′UTR (“del2.5”) that disrupts miRNA-binding sites and is associated with lifelong low LDL-C levels. This review summarizes recent advances, mechanisms of action, clinical progress, and remaining challenges across antisense oligonucleotides, siRNAs, gene therapy, genome editing, and emerging miRNA-based therapeutics for hypercholesterolemia. As an example of the latter approach, the liver-directed miR-30c analog C2 has demonstrated preclinical activity by coordinately reducing hepatic lipoprotein secretion and lipogenesis while enhancing cholesterol elimination, resulting in reduced LDL-C and atherosclerosis. However, it must be noted that these findings remain preclinical, and further optimization of delivery, pharmacokinetics, safety, and long-term efficacy will be required before clinical evaluation. Continued advances in RNA chemistry, targeted delivery, and genome engineering are expected to further expand the therapeutic landscape for dyslipidemia and cardiovascular disease. Full article

(This article belongs to the Special Issue The Evolving Landscape of Cell and Gene Therapy—Opportunities, Challenges and the Road Ahead)

35 pages, 2974 KB

Open AccessReview

Extracellular Vesicle-Mediated Macrophage Polarization in Sepsis-Induced Acute Lung Injury: Molecular Mechanisms and Therapeutic Opportunities

by Yiqian Shen, Yi Tai, Xinzhe Liu, Yang Li, Zihao Zhao, Xuejun Jin and Juan Ma

Cells 2026, 15(17), 1574; https://doi.org/10.3390/cells15171574 - 29 Aug 2026

Sepsis-induced acute lung injury (SI-ALI) is a severe complication of sepsis characterized by dysregulated inflammatory responses and impaired immune homeostasis. Growing evidence indicates that extracellular vesicles (EVs), particularly exosomes, are important mediators of intercellular communication. Despite the heterogeneity of infectious sources underlying sepsis, [...] Read more.

Sepsis-induced acute lung injury (SI-ALI) is a severe complication of sepsis characterized by dysregulated inflammatory responses and impaired immune homeostasis. Growing evidence indicates that extracellular vesicles (EVs), particularly exosomes, are important mediators of intercellular communication. Despite the heterogeneity of infectious sources underlying sepsis, EVs can regulate macrophage polarization and functional reprogramming by transferring diverse bioactive cargo. Consequently, EVs are involved in the pathophysiological progression of SI-ALI arising from sepsis of different etiologies. However, the mechanisms through which distinct EV cargos regulate macrophage function and contribute to SI-ALI pathogenesis remain incompletely understood. To address these issues, this review summarizes how different EV subtypes and their cargos, including RNAs, proteins, lipids, and DNA, modulate macrophage functional states through multiple signaling pathways. The effect of such processes further contributes to inflammatory reaction, immune balance, and tissue regeneration in acute lung injury caused by damage to the SI-ALI. Particularly, the EV-mediated modulation of macrophage function goes beyond the rigid M1/M2 dichotomy, being rather based on the dynamic functional repertoire involving both pro-inflammatory response and immune regulation as well as tissue regeneration. The article finally concludes with EV-based treatment approaches aimed at cargo delivery or blocking and the main problems related to translational medicine. Overall, the review article identifies the macrophage regulatory network controlled by EVs, thus helping to understand immunopathogenesis of SI-ALI as well as laying the theoretical foundation for developing EV-based precision medicine. Full article

(This article belongs to the Section Cellular Immunology)

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25 pages, 1269 KB

Open AccessArticle

Genome-Resolved Functional Profiling of Osteoporosis-Associated Gut Bacteria Highlights Putative Metabolic and Immunogenic Signatures of the Gut–Bone Axis

by Rogelio F. Jiménez-Ortega, Alejandra I. Ortega-Meléndez, Juan F. Montes-García, Erasmo Negrete-Abascal, Nelly Patiño, Eric G. Ramírez-Salazar, Rosalba Sevilla-Montoya, Rafael Velázquez-Cruz and Alberto Hidalgo-Bravo

Cells 2026, 15(17), 1573; https://doi.org/10.3390/cells15171573 - 29 Aug 2026

The gut microbiota has emerged as a potential regulator of bone metabolism, but the genome-encoded functional repertoire of osteoporosis-associated gut bacteria remains insufficiently characterized. This study performed in silico functional profiling of gut bacterial taxa associated with osteoporosis, low bone mineral density, or [...] Read more.

The gut microbiota has emerged as a potential regulator of bone metabolism, but the genome-encoded functional repertoire of osteoporosis-associated gut bacteria remains insufficiently characterized. This study performed in silico functional profiling of gut bacterial taxa associated with osteoporosis, low bone mineral density, or comparator bone-related phenotypes. Twenty candidate taxa were selected from evidence in the human microbiome and represented by 26 curated bacterial reference genomes. Genome-wide annotations were used to map predicted gut–bone axis signatures, carbohydrate-active enzyme (CAZyme) repertoires, selected Kyoto Encyclopedia of Genes and Genomes pathways, and gutSMASH-predicted metabolic gene clusters. Functional burdens were normalized as hits per 1000 annotated proteins and integrated into metabolic, immunogenic, CAZyme, KEGG, and metabolic gene cluster profiles. Twelve predicted gut–bone axis signatures were identified, comprising 3337 primary candidate protein hits and a strict high-confidence subset of 2497 hits. Dominant signatures included vitamin B12/cobalamin metabolism, folate/one-carbon metabolism, peptidoglycan/cell-wall biosynthesis, and short-chain fatty acid-related functions. Dialister invisus, Dialister succinatiphilus, Megamonas funiformis, and Megamonas hypermegale showed the strongest normalized predicted gut–bone axis signal. These hypothesis-generating findings prioritize microbial metabolic and immunogenic features for future metagenomic, metabolomic, and experimental validation studies. Full article

(This article belongs to the Topic Bone-Related Diseases: From Molecular Mechanisms to Therapy Development—2nd Edition)

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9 pages, 1183 KB

Open AccessCommunication

Establishment of a 3D Co-Culture System Using OFT Cell Line and Effect of Hormone Supplementation on Germline Gene Expression in Olive Flounder (Paralichthys olivaceus)

by Jae Hoon Choi, Hee Jeong Kong and Jung-Ha Kang

Cells 2026, 15(17), 1572; https://doi.org/10.3390/cells15171572 - 29 Aug 2026

In vitro 3D cell culture systems provide a physiologically relevant microenvironment that mimics native tissue architecture. However, establishing functional 3D testicular aggregates in teleosts remains challenging. In this study, we established a novel 3D co-culture aggregate system for olive flounder (Paralichthys olivaceus [...] Read more.

In vitro 3D cell culture systems provide a physiologically relevant microenvironment that mimics native tissue architecture. However, establishing functional 3D testicular aggregates in teleosts remains challenging. In this study, we established a novel 3D co-culture aggregate system for olive flounder (Paralichthys olivaceus) primary testicular cells by incorporating the established olive flounder testicular cell (OFT) line. Primary testicular cells alone failed to form 3D aggregates within the first 24 h in ultra-low attachment plates. However, co-culturing with OFT cells rapidly initiated 3D aggregate assembly within 24 h. Furthermore, supplementation with a cocktail of sex hormones and growth factors maintained high cell viability without cytotoxic effects. Notably, quantitative real-time PCR analysis revealed that hormone and growth factor supplementation significantly upregulated the transcript levels of both plzf (2.15-fold) and scp3 (2.34-fold). These results demonstrate that the OFT cell line is essential for facilitating the assembly and incorporation of primary testicular cells into 3D aggregates, while sex hormones and growth factors promote spermatogonial stem cell maintenance and meiotic progression within the aggregates. Overall, this 3D co-culture platform serves as a valuable in vitro tool for fish spermatogonial stem cell research and reproductive biotechnology in aquaculture. Full article

(This article belongs to the Special Issue Cellular and Molecular Mechanisms in Reproductive Biology and Fertility)

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29 pages, 7063 KB

Open AccessReview

Lactate Metabolism and Signaling in Amyotrophic Lateral Sclerosis

by Xiaonan Ma, Jinmeng Liu, Yingjun Guan, Chunjie Xu, Mu Li, Xue Zhang, Zongze Li, Lanli Zhang, Xuemei Wang, Haoyun Zhang and Yanchun Chen

Cells 2026, 15(17), 1571; https://doi.org/10.3390/cells15171571 - 29 Aug 2026

Amyotrophic lateral sclerosis (ALS) is a progressive and fatal neurodegenerative disease characterized by the selective degeneration of upper and lower motor neurons (MNs). Although the specific pathogenesis of ALS is not yet fully understood, there is increasing evidence that abnormal energy metabolism plays [...] Read more.

Amyotrophic lateral sclerosis (ALS) is a progressive and fatal neurodegenerative disease characterized by the selective degeneration of upper and lower motor neurons (MNs). Although the specific pathogenesis of ALS is not yet fully understood, there is increasing evidence that abnormal energy metabolism plays a key role in the onset and progression of the disease. Lactate has traditionally been considered a metabolic by-product of glycolysis and has received increasing attention in recent years. Research has shown that lactate is not only an important energy substrate but also a signaling molecule that regulates a variety of physiological processes, including neuron-glia metabolic coupling, neuroprotection and inflammatory responses. In ALS, abnormalities in lactate metabolism, dysfunction of the lactate shuttle, and dysregulation of lactate-related signaling pathways may jointly lead to neuronal energy deficits and increased neuroinflammation, thereby promoting MN degeneration. This review summarizes the latest advances in lactate metabolism and lactate-mediated signaling in ALS, with particular emphasis on their roles in neuronal energy regulation, neuroprotection and inflammatory regulation. In addition, we also discuss potential therapeutic strategies for lactate metabolism and its related pathways, aiming to provide new insights into the pathogenesis of ALS and the development of treatment methods for lactate-related metabolism. Full article

(This article belongs to the Special Issue Role of Gene Regulation in Neurological Disorders)

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20 pages, 4050 KB

Open AccessArticle

Schwann Cell Activity in the Multiple Sclerosis Microenvironment

by Michael R. Shurin, Galina V. Shurin, Carolina Moreira Doyle, Anna E. Lokshin and Sarah E. Wheeler

Cells 2026, 15(17), 1570; https://doi.org/10.3390/cells15171570 - 29 Aug 2026

Schwann cell (SC)-based therapy is currently being debated as an approach to promote functional recovery in patients with multiple sclerosis (MS) and other inflammatory demyelinating diseases of the central nervous system (CNS). The main limitation of SC transplantation in MS patients is the [...] Read more.

Schwann cell (SC)-based therapy is currently being debated as an approach to promote functional recovery in patients with multiple sclerosis (MS) and other inflammatory demyelinating diseases of the central nervous system (CNS). The main limitation of SC transplantation in MS patients is the short-term functional activity of SCs in the CNS environment. The goal of this study was to determine phenotypic, functional, and signaling changes in human SCs treated with CSF samples from MS patients in vitro, and to characterize the molecular mechanisms underlying SC injury response in the model MS microenvironment. We demonstrated that SC proliferation and motility were suppressed, while the expression of both pro-myelinating genes and negative regulators of myelination was up-regulated in cells incubated with CSF from MS patients. This was associated with active phosphorylation of ERK and c-Jun, and inhibition of these signaling pathways prevented SC changes. The overall analysis of detected abnormalities and SC markers indicates that SCs do not exhibit either a ‘classic’ dedifferentiation-repair-like phenotype or a myelin-forming maturation phenotype when placed in MS-like conditions. They demonstrate an uncommon pattern of cellular signaling reprogramming, associated with decreased motility and potentially decreased myelination. We thus suggest that ERK- and JNK-modulated SCs should be further investigated as a potential cell source for CNS repair in MS. Full article

(This article belongs to the Special Issue Remyelination: From Molecular Mechanism to Therapy)

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