ArticleWorld journal of stem cells2025
Reduced NRF2/Mfn2 activity promotes endoplasmic reticulum stress and senescence in adipose-derived mesenchymal stem cells in hypertrophic obese mice.
Article in World journal of stem cells, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Hyperbaric Oxygen Attenuates Cerebral Ischemia-Reperfusion Injury Through ROS-Dependent Remodeling of Microglial Mitochondrial Dynamics.International journal of molecular sciences · 2026Article
- Insights into mitofusin-2 and endoplasmic reticulum stress regulation in adipose-derived mesenchymal stem cells senescence.World journal of stem cells · 2025Article
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Abstract
backgroundHypertrophy obesity is closely associated with obesity-related metabolic diseases. The senescence of adipose-derived mesenchymal stem cells (ASCs) is believed to play a significant role in the development of hypertrophy obesity.
aimTo investigate the relationship between ASC senescence, endoplasmic reticulum (ER) stress, and nuclear factor erythroid-derived 2 (NRF2) activity in a mouse model of hypertrophy obesity. Additionally, we explored the mechanism through which NRF2 affects ASC senescence
methodsWe observed the senescent phenotype and ER stress (ERS) in ASCs from hypertrophic obese mouse models, and determined NRF2 activity. Chromatin immunoprecipitation-quantitative polymerase chain reaction (qPCR) was used to analyze the transcriptional activity of NRF2 on
resultsThe study found significant increases in senescence and ERS, accompanied by decreased NRF2 activity in ASCs from hypertrophic obese mouse models. Simultaneously, chromatin immunoprecipitation-qPCR analysis revealed a reduction in NRF2 transcriptional activity on
conclusionThe research outcomes suggest that NRF2 may regulate ERS and senescence in subcutaneous ASCs of hypertrophic obese mice by modulating
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