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Cells, Volume 15, Issue 8 (April-2 2026) – 5 articles

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21 pages, 1018 KB

Open AccessArticle

Arsenic-Induced PPARγ, with the Coordinated Action of p62, Inhibits Apoptosis and Necroptosis and Activates the DNA Damage Response in A549 Lung Cancer Cells, Leading to Carcinogenesis

by Hak-Ryul Kim and Seon-Hee Oh

Cells 2026, 15(8), 659; https://doi.org/10.3390/cells15080659 - 8 Apr 2026

Abstract

Arsenic exposure increases lung cancer risk, yet its molecular mechanisms remain unclear but are linked to peroxisome proliferator-activated receptor gamma (PPARγ). We investigated PPARγ-related molecules affected by sodium arsenite (NaAR) in non-small cell lung cancer (NSCLC) cells using immunochemical, gene knockdown, and immunoprecipitation approaches. PPARγ was critical for NSCLC growth, as high PPARγ-expressing A549 cells proliferated more than low-expressing H1299 cells after NaAR treatment. In A549 cells, NaAR upregulated polyubiquitinated PPARγ, activating cell cycle arrest and DNA damage response pathways. Rather than inducing significant caspase-dependent apoptosis, NaAR activated nuclear factor-kappa B and downregulated mixed lineage kinase domain-like (MLKL) via K63-linked polyubiquitinated receptor-interacting protein kinase 1, thereby inhibiting apoptosis and necroptosis. PPARγ knockdown or NAD⁺ supplementation induced PARP-1 hyperactivation and MLKL upregulation, leading to DNA damage and necroptosis. PARP-1 inhibition by 3-aminobenzamide induced apoptosis, indicating that PPARγ regulates apoptosis and necroptosis through PARP-1 activation. Proteasome inhibition increased polyubiquitinated PPARγ but not p53. Leptomycin B induced PPARγ degradation and p53 accumulation, promoting necroptosis and apoptosis, suggesting cytoplasmic p53 contributes to cell death. p62 interacted with PPARγ and p53, and its knockdown suppressed their NaAR-induced upregulation. In conclusion, NaAR-induced PPARγ promotes A549 cell survival by enhancing DNA repair and inhibiting apoptosis and necroptosis via cooperation with p53 and p62, highlighting PPARγ as a potential therapeutic target. Full article

(This article belongs to the Special Issue Toxicology in Cells: Cellular Mechanisms, Molecular Responses, and Modern Models)

15 pages, 801 KB

Open AccessReview

H19/miR-675 Axis Promotes Cancer Metastasis by Orchestrating EMT and MET Processes

by Kekely Klouyovo, Xuefen Le Bourhis and Éric Adriaenssens

Cells 2026, 15(8), 658; https://doi.org/10.3390/cells15080658 - 8 Apr 2026

Abstract

Despite substantial advances in our understanding of cancer metastasis, it remains the leading cause of mortality among cancer patients. Elucidating the molecular mechanisms that drive metastatic progression is expected to facilitate the development of more effective therapeutic strategies. Among the numerous candidates, the long non-coding RNA H19 and its derivative miR-675 have been increasingly recognized as key regulators of metastatic dissemination in cancers of diverse tissue origins. In this review, we provide an up-to-date overview of the H19/miR-675 axis in metastatic progression, with particular emphasis on its involvement in the dynamic and complementary processes of epithelial–mesenchymal transition (EMT) and mesenchymal–epithelial transition (MET). We also highlight the opportunity to consider the H19/miR-675 axis as promising biomarkers and potential therapeutic targets. Full article

34 pages, 1874 KB

Open AccessReview

Immunosenescence and Inflammaging as Drivers of Neurodegeneration: Cellular Mechanisms, Neuroimmune Crosstalk, and Therapeutic Implications

by Gianmarco Bertoni, Sara Ristori and Daniela Monti

Cells 2026, 15(8), 657; https://doi.org/10.3390/cells15080657 - 8 Apr 2026

Abstract

Aging is accompanied by profound alterations in immune function, termed immunosenescence, and by a chronic, low-grade inflammatory state known as inflammaging. These processes are increasingly recognized as central drivers of age-related neurodegenerative diseases, including Alzheimer’s Disease, Parkinson’s Disease, Amyotrophic Lateral Sclerosis and Multiple Sclerosis. In the central nervous system, senescent microglia and astrocytes lose their homeostatic and neuroprotective functions, while systemic immune aging and blood–brain barrier dysfunction further amplify neuroinflammation and impair protein aggregate clearance. This sustained pro-inflammatory environment promotes synaptic dysfunction, neuronal loss and cognitive decline. Here, we synthesize current knowledge of the mechanistic links among immunosenescence, inflammaging, and neurodegeneration, highlighting innate and adaptive immune dysregulation, mitochondrial impairment, and failed resolution pathways. We further discuss emerging therapeutic strategies, including senolytics, immunoceuticals, microbiome-based interventions and advanced drug delivery systems, aimed at restoring immune homeostasis and enhancing brain resilience. By integrating mechanistic and translational insights, this review provides a framework for developing novel interventions to target immune aging in neurodegenerative diseases. Full article

(This article belongs to the Special Issue Targeting Immune Dysfunction in Aging and Age-Related Diseases)

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28 pages, 625 KB

Open AccessReview

Stem Cells and Their Derivatives in Cardiac Fibrosis Therapy: Challenges and Perspectives

by Adrian Piwowar, Zuzanna Zolbach, Julia Rydzek, Natalia Skonieczna, Katarzyna Rojek, Mateusz Żołyniak, Julia Soczyńska and Sławomir Woźniak

Cells 2026, 15(8), 656; https://doi.org/10.3390/cells15080656 - 8 Apr 2026

Abstract

Cardiac fibrosis is a pathology induced by various conditions, such as myocardial infarction, or certain cardiomyopathies, and represents one of the most prevalent cardiac abnormalities. This process, defined as the excessive accumulation of extracellular matrix within damaged cardiac tissue, leads to significant complications, including impaired systolic and diastolic function as well as arrhythmias. Conventional therapies focus primarily on slowing down the progression of fibrosis. Recently, there has been a growing research interest in therapies based on stem cells and their derivatives, which hold the potential to greater decrease formation and area of fibrosis. In this review, we aim to systematise the most recent data regarding the application of these approaches. We focus on describing the types of cells employed, methods of their implementation, and strategies for optimising these processes. Particular attention is given to exosomes due to the reports highlighting their use as innovative and potentially effective tools in the treatment of cardiac diseases. Full article

(This article belongs to the Section Cells of the Cardiovascular System)

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19 pages, 15696 KB

Open AccessArticle

From Phage Display to Yeast Secretion: Developing Fc-Fused Nanobodies Against Influenza Virus

by Mei Wang, Shujun Li, Yong Li, Xiaomei Xia, Yan Zhang, Ning Cao, Yuanfang Li, Yijia Liu, Sheng Zhang, Lilin Zhang and Jinhai Huang

Cells 2026, 15(8), 655; https://doi.org/10.3390/cells15080655 - 8 Apr 2026

Abstract

Avian influenza infections cause substantial economic losses in the poultry industry and raise public health concerns due to viral adaptation and cross-species transmission. The frequent antigenic drift of influenza viruses further complicates the prevention and treatment of avian respiratory infections. In this study, we generated high-affinity heavy-chain variable domain (VHH) nanobodies from naïve alpaca/camelid VHH libraries using phage display combined with H9N2 influenza A virus (IAV)-infected Madin-Darby Canine Kidney (MDCK) cells. Based on binding affinity and neutralization potential, we identified seven hemagglutinin (HA)-specific and two neuraminidase (NA)-specific VHHs. Molecular docking predicted the interaction sites of HA-specific VHHs (L1-2, L1-4, A5) and NA-specific VHHs (L1-3, L2-2), providing mechanistic insights. Notably, the three HA-specific VHHs (L1-2, L1-4, A5) showed cross-reactivity to representative HA subtypes (H1, H3, and influenza B), indicating recognition of conserved epitopes across divergent influenza strains. For the first time, these camelid nanobodies were fused to the chicken IgY Fc domain, and the expression cassette was integrated into the Saccharomyces cerevisiae genome, achieving a secretion yield of 15–20 mg/L of VHH-Fc antibodies. Experimental validation confirmed that the three HA-specific VHHs-Fc constructs effectively blocked viral infection, while the two NA-specific VHH-Fc constructs (L1-3, L2-2) inhibited NA activity, demonstrating the functional efficacy of the yeast-secreted VHH–IgY Fc platform. This novel IgY Fc fusion approach offers a scalable platform with enhanced stability, extended circulation potential, and applicability in poultry. Full article

(This article belongs to the Topic Advances in Vaccines and Antimicrobial Therapy—2nd Edition)

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