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Published on: June 14, 2016
Sirtuins as Endogenous Regulators of Cardiac Fibrosis: A Current Perspective
Zeinab Farhadi1, Mansour Esmailidehaj1, Shahab Masoumi2,3
1Yazd Neuroendocrine Research Center, School of Medicine, Shahid Sadoughi University of Medical Sciences and Health Services, Yazd, 8915173149, Iran.
Insights
Sirtuins (SIRTs) are key regulators of cardiac fibrosis, a condition leading to heart failure. Targeting SIRTs offers promising therapeutic strategies for treating cardiac fibrosis and related cardiovascular diseases.
Area of Science:
- Cardiovascular Research
- Molecular Biology
- Biochemistry
Background:
- Cardiac fibrosis, characterized by excessive extracellular matrix accumulation, severely impairs heart function and contributes to heart failure.
- Current treatments for cardiac fibrosis are limited due to its complex pathogenesis and heterogeneous causes.
- Sirtuins (SIRTs), a family of NAD+-dependent deacetylases, are crucial in regulating cellular processes linked to cardiac fibrosis, including oxidative stress, inflammation, and metabolism.
Purpose of the Study:
- To comprehensively review the roles of the seven mammalian sirtuins (SIRT1-SIRT7) in the pathogenesis and progression of cardiac fibrosis.
- To highlight sirtuins as potential molecular targets for novel anti-fibrotic therapies.
- To explore the therapeutic potential of sirtuin activators in mitigating cardiac fibrosis.
Main Methods:
- Literature review of existing clinical and experimental evidence on sirtuins and cardiac fibrosis.
- Analysis of the molecular mechanisms by which sirtuins influence cardiomyocyte function and extracellular matrix homeostasis.
- Discussion of the translational applications of targeting sirtuins for cardiac fibrosis treatment.
Main Results:
- Sirtuins play critical roles in regulating key cellular processes implicated in cardiac fibrosis, such as oxidative stress, inflammation, energy metabolism, mitochondrial function, and epithelial-to-mesenchymal transition (EMT).
- Evidence suggests that sirtuin activators, including resveratrol and NAD+ precursors, may hold therapeutic potential in reducing cardiac fibrosis.
- The complex and context-dependent functions of sirtuins in cardiac fibrosis require further investigation.
Conclusions:
- Sirtuins are integral to the development and progression of cardiac fibrosis.
- Targeting sirtuins presents a promising avenue for developing innovative anti-fibrotic therapies.
- Further research into sirtuin mechanisms is essential for advancing the treatment of cardiac fibrosis and associated cardiovascular diseases.
Abstract:
Cardiac fibrosis is a pathological condition marked by the excessive accumulation of extracellular matrix (ECM) components, which leads to impaired cardiac function and heart failure. Despite its significant contribution to cardiovascular morbidity and mortality, no effective therapeutic drugs specifically target the inhibition of cardiac fibrosis, largely due to the complex etiological heterogeneity and pathogenesis of this disease. Sirtuins (SIRTs), a family of NAD + -dependent deacetylases, play a critical role in cellular processes such as oxidative stress, inflammation, energy metabolism, mitochondrial function, epithelial-to-mesenchymal transition (EMT), and ECM homeostasis, all of which are implicated in cardiac fibrosis. Growing clinical and experimental evidence suggests that SIRTs regulate the cellular and molecular mechanisms of cardiomyocytes through various biological pathways. Emerging evidence indicates that sirtuin activators, including resveratrol and NAD + precursors, hold therapeutic potential in mitigating cardiac fibrosis. However, the complex and context-dependent roles of sirtuins necessitate further research to fully elucidate their mechanisms and translational applications. As the role of SIRTs in relation to cardiac fibrosis and its associated mechanisms is rarely discussed in the literature, this review comprehensively addresses the roles of the seven mammalian sirtuins (SIRT1-SIRT7) in the pathogenesis and progression of cardiac fibrosis. It highlights the key role of SIRTs as molecular targets for innovative anti-fibrotic therapies, offering new avenues for the treatment of cardiac fibrosis and associated cardiovascular diseases.
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