ArticleCell death & disease2025
MSCs ameliorates hyperglycemia-induced endothelial injury through modulation of mitochondrial dynamics.
Article in Cell death & disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- From Adaptive Resilience to Catastrophic Systems Collapse: Endothelial Entropy, Ferroptotic Propagation, and the Maternal Point of No Return in Emergency Peripartum Hysterectomy.International journal of molecular sciences · 2026Review
- Mitochondrial dysfunction in endothelial senescence: implications for vascular remodeling and therapeutic strategies.Archives of pharmacal research · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
Endothelial dysfunction contributes to the development of cardiovascular disease in patients with diabetes mellitus, and current strategies remain inadequate. Although mesenchymal stromal cells (MSCs) have shown beneficial effects in experimental models of diabetes, underlying mechanisms remain elusive. Here, using a human umbilical vein endothelial cells (HUVECs) treated with high concentration of glucose (HG) and a mouse model of type 2 diabetes (db/db mice), we demonstrate MSCs could alleviate hyperglycemia-induced endothelial injury by preventing aberrant mitochondrial morphology. Mechanistically, stanniocalcin-1(STC1) was identified to be an important paracrine factor secreted by MSCs, which restrains hyperactivation of ERK1/2, thus preventing Drp1-mediated excessive mitochondrial fission, and thereby protecting against hyperglycemia-induced oxidative injury, endothelial inflammation and mitochondrial apoptotic pathway, consequently protecting endothelial dysfunction. Hence, this study reveals that MSCs-derived STC1 regulates mitochondrial dynamics remodeling through inhibiting ERK1/2-Drp1 axis and provide a therapeutic target in diabetic vasculopathy and regenerative medicine.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.