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Cellular senescence, a process that induces irreversible cell cycle arrest in response to diverse stressors, is a primary contributor to aging and age-related diseases. Currently, exposure to hydrogen peroxide is a widely used technique for establishing in vitro cellular senescence models; however, this traditional method is inconsistent, laborious, and ineffective in vivo. To overcome these limitations, we have developed a hydrogen peroxide-releasing hydrogel that can readily and controllably induce senescence in conventional 2-dimensional cell cultures as well as advanced 3-dimensional microphysiological systems. Notably, we have established 2 platforms using our hydrogen peroxide-releasing hydrogel for investigating senolytics, which is a promising innovation in anti-geronic therapy. Conclusively, our advanced model presents a highly promising tool that offers a simple, versatile, convenient, effective, and highly adaptable technique for inducing cellular senescence. This innovation not only lays a crucial foundation for future research on aging but also markedly accelerates the development of novel therapeutic strategies targeting age-related diseases.
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http://dx.doi.org/10.34133/bmr.0161 | DOI Listing |
Biomaterials
August 2025
Department of Oral and Cranio-maxillofacial Surgery, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, College of Stomatology, Shanghai Jiao Tong University, National Center for Stomatology, National Clinical Research Center for Oral Diseases, Shanghai Key Laborator
Bone healing requires Schwann cells (SCs) paracrine factors for mesenchymal stem cell function. Diabetes mellitus (DM) patients are susceptible to developing SCs dysfunction and impairing bone healing. Rare research considered reconstructing mesenchymal stem cell-schwann cell circuitry in diabetic bone regeneration.
View Article and Find Full Text PDFJ Nutr Biochem
September 2025
Department of Woman-Mother-Child, Division of Pediatrics, DOHaD Laboratory, University of Lausanne and Lausanne University Hospital, 1011 Lausanne, Switzerland. Electronic address:
Background: Individuals born after intrauterine growth restriction (IUGR) have a higher risk of developing metabolic syndrome (MetS) in adulthood. In a rat model, male IUGR offspring exhibit MetS features-including elevated systolic blood pressure, glucose intolerance, non-alcoholic fatty liver disease, and increased visceral adipose tissue (VAT)-by 6 months of age. Female offspring, however, do not.
View Article and Find Full Text PDFInt Immunopharmacol
September 2025
Department of Medical Science Research Center, Brain Injury and Drug Prevention Research Key Laboratory of Shaanxi Universities, Peihua University, Xi'an, Shaanxi 710125, China; Department of Neurosurgery, Bijie Traditional Chinese Medicine Hospital, Bijie 551700, China; School of Life and Health Sc
The incidence of traumatic brain injury (TBI) has demonstrated a marked escalation recently. Nevertheless, there remains a critical paucity of effective drug interventions targeting persistent neuroinflammation-induced damage following TBI. STING/NF-κB axis-induced pyroptosis emerges as a pivotal mechanism driving persistent neuroinflammation, providing it as a potential target for multi-pathway precision therapeutic in TBI.
View Article and Find Full Text PDFRedox Biol
September 2025
Department of Spine Surgery, The Second Affiliated Hospital of Nantong University, Nantong First People's Hospital, Medical School of Nantong University, Nantong, Jiangsu, 226000, China; Research Institute for Spine and Spinal Cord Disease of Nantong University, Nantong, Jiangsu, 226000, China. Elec
Spinal cord injury (SCI) is a devastating condition characterized by the accumulation of myelin debris (MD), persistent neuroinflammation, and impaired neural regeneration. Although macrophages are pivotal for MD clearance, the impact of excessive MD phagocytosis on macrophage phenotype and function remains poorly understood. Building upon our prior evidence that exendin-4 (Ex-4), a glucagon-like peptide-1 receptor (GLP-1R) agonist, mitigates microglia-driven neuroinflammation post-SCI, this study elucidates the therapeutic efficacy and underlying mechanisms of Ex-4 in alleviating macrophage senescence, restoring efferocytotic capacity, and facilitating neural repair.
View Article and Find Full Text PDFDiabetes Metab Res Rev
September 2025
Department of Nephrology, Daping Hospital, Army Medical University, Chongqing, China.
Chronic kidney disease (CKD) substantially increases cardiovascular risk, with endothelial dysfunction as its central pathological mechanism. This review summarises the molecular regulatory mechanisms underlying endothelial dysfunction in CKD and highlights recent advances in treatment strategies. The pathophysiology of endothelial injuries involves a complex network of multiple factors and mechanisms, including oxidative stress, inflammation, glycocalyx damage, ischaemia, hypoxia, cellular senescence and endothelial-mesenchymal transition (EndMT).
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