ArticleIranian journal of basic medical sciences2025
SIRT5 prevents mitochondrial dysfunction and cardiac hypertrophy induced by RIP140.
Article in Iranian journal of basic medical sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- SIRT5 Attenuates Doxorubicin-Induced Acute Cardiac Injury by Modulating PHB2 Succinylation and the Mitophagic Response.Cardiovascular toxicology · 2026Article
- The spleen-heart crosstalk in cardiovascular disease: integrating neural, immune, and secretory pathways.Acta pharmacologica Sinica · 2026Review
- Unveiling the importance of SIRT5 for cardiac health and disease in an era of increasing longevity.GeroScience · 2026Review
- SIRT1: The first key to unlocking the mystery of cardiovascular diseases.Frontiers in pharmacology · 2025Review
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Authors and funding
6 authors.
Funding
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Abstract
Objectives: To investigate the effect and mechanism of sirtuin5 (SIRT5) on mitochondrial dysfunction and cardiac hypertrophy induced by receptor-interacting protein 140 (RIP140). Materials and Methods: The neonatal rat cardiomyocytes (NRCMs) and SD rats were treated with Angiotensin II (Ang II) to induce Results: The expression of SIRT5 was down-regulated in NRCMs and hearts treated with Ang II. Overexpression of SIRT5 protected cardiomyocytes from AngII-induced hypertrophy, whereas knockdown of SIRT5 resulted in cardiac hypertrophy. Moreover, since SIRT5 was regulated by the transcriptional coactivator, we also found that SIRT5 could be negatively regulated by the transcriptional corepressor RIP140 in cardiomyocytes. Furthermore, SIRT5 significantly attenuated energy metabolic dysregulation and mitochondrial dysfunction and exerted its protective role on myocardial hypertrophy under the regulation of RIP140. Conclusion: SIRT5 exerts a protective role in mitochondrial dysfunction and cardiac hypertrophy induced by RIP140.
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