ArticleApoptosis : an international journal on programmed cell death2026
Reparative effects of VCAM-1 high-performance MSC-derived exosomes on aged diabetic cardiomyocyte injury: a focus on ferroptosis suppression.
Article in Apoptosis : an international journal on programmed cell death, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Small Extracellular Vesicles in Cardioprotection, Cardiac Repair, and Regeneration: Cargo Mechanisms, Producer Cell Sources, and Translational Development.Biomedicines · 2026Review
- Advances in the application of nanoparticles for the diagnosis and treatment of diabetic cardiomyopathy.Frontiers in cell and developmental biology · 2026Review
- Pathogenesis of diabetic cardiomyopathy and emerging therapeutic strategies: a network-based perspective.Frontiers in clinical diabetes and healthcare · 2026Review
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Authors and funding
8 authors.
Funding
Abstract
Cardiac dysfunction in elderly diabetes, due to superimposition of age-related myocardial senescence and diabetes-induced injury, lacks effective therapeutic strategies. Ferroptosis may be a key mechanism underlying cardiomyocyte injury in diabetic cardiomyopathy. Mesenchymal stem cells (MSCs) and their exosomes show potential for repairing cardiomyocytes, restoring cardiac function, improving insulin sensitivity, and mitigating diabetes-related complications, but their mechanisms and relationship with ferroptosis remain unclear. The present study aimed to investigate reparative effects and ferroptosis-mediated mechanism of exosomes derived from VCAM-1 high-performance MSCs on aged diabetic cardiomyocyte injury. High-glucose-damaged senescent cardiomyocyte and aged rat model of diabetic cardiomyopathy were established and treated with VCAM-1⁺-UC-MSCs or -derived exosomes. Assessments of cell phenotypes, RNA sequencing, cardiac function, and markers of senescence and ferroptosis revealed significant mitochondrial damage, iron-ion accumulation, reactive oxygen species (ROS), and cardiac troponin (c-TnT) elevation in the damaged myocardial cells and rat heart tissues, along with weakened cardiac function and pronounced senescence and ferroptosis features, and activation of Ras/Raf/MEK/ERK/c-FOS pathway. VCAM-1⁺ MSCs or exosome administration significantly alleviated these effects, and improved cardiac function. Notably, the reparative effect of VCAM-1⁺-UC-MSCs-derived exosomes was superior to that of conventional MSCs-derived exosomes. In conclusion, VCAM-1⁺-UC-MSCs-derived exosomes attenuate cardiomyocyte ferroptosis by suppressing Ras/Raf/MEK/ERK/c-FOS pathway, thereby ameliorating myocardial injury resulting from superimposition of aging-caused myocardial senescence and diabetes-induced damage in elderly diabetic cardiomyopathy. This may lay a foundation for identifying potential prevention and treatment strategies and targets of MSCs and -derived exosomes on myocardial injury.
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