Circ-Hipk3 in Adipose Derived Stem Cells Exosome Alleviates Myocardial Infarction Induced Myocardial Damage by Regulation miR-138-5p/Sirt1 Axis Mediated Autophagy.
Yang G., Nong D., Tang X., Tan L., Yang P., Ning H.
Animal Study on Cardiovascular Disease, Chronic Inflammation, published in Biochem Genet (2025) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
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- Study type
- Animal Study
- Journal
- Biochem Genet (2025)
- Country
- United States
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 40696229
- DOI
- 10.1007/s10528-025-11173-5
Abstract (original English)
Myocardial infarction (MI) is a major health problem and is the leading cause of death worldwide. Accumulation studies confirm that exosomes derived from stem cells have been shown to effectively repair MI injury-induced cardiomyocyte damage. However, the cardioprotective benefits of adipose tissue-derived mesenchymal stem cell (ADSC)-Exos remain unclear. This study aimed to investigate the protective effects of exosomes from ADSC on the hearts of MI-treated mice and to explore the underlying mechanisms. Cellular and molecular mechanisms were investigated using cultured ADSCs. On C57BL/6 J mice, we performed myocardial MI model. HMEC-1 was used to identify the regulatory mechanism. ELISA was used for inflammatory factor expression detection. Luciferase report analysis detection showed the relationship among miR-138-5p, Sirt1 and circ-Hipk3. ADSCs exosome treatment significantly alleviates MI induced myocardial damage by promotion autophagy and inhibits inflammatory response. Circ-Hipk3 play an important role in ADSCs exosome mediated protective effect on MI induced myocardial damage. Luciferase report analysis confirmed that miR-138-5p and SIRT1 were at circ-Hipk3 downstream. Downregulation SIRT1 or upregulation miR-138-5p reversed the regulation effect of circ-Hipk3 on autophagy and inflammatory factor expression. Overexpression circ-Hipk3 increased the protective effect of AD
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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