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Abstract
Sirtuins are involved in regulating myocardial fibrosis, a key feature of heart failure.
- SIRT1, SIRT3, and SIRT6 may inhibit fibroblast activation and reduce oxidative and inflammatory damage.
- SIRT4 could promote fibrosis depending on the specific context.
- The review discusses the role of non-coding RNAs and histone modifications in regulating sirtuin expression.
- There is a complex feedback between sirtuins and processes like mitochondrial balance and endothelial-to-mesenchymal transition.
- Sirtuins are positioned as potential therapeutic targets for cardiac fibrosis due to their dual roles.
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