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Updated: Sep 16, 2025

Deacetylation Assays to Unravel the Interplay between Sirtuins SIRT2 and Specific Protein-substrates
Published on: February 27, 2016
SIRT3 as a potential biomarker and therapeutic target for cardiovascular diseases: a meta-analysis of clinical
Nikhil Gupta1, Vikas Kumar1, Abhinav Kanwal1
1Department of Pharmacology, All India Institute of Medical Sciences, Bathinda, India.
Insights
Sirtuin 3 (SIRT3) levels are significantly lower in cardiovascular disease (CVD) patients. This finding highlights SIRT3
Area of Science:
- Mitochondrial biology
- Cardiovascular research
- Biomarker discovery
Background:
- Cardiovascular diseases (CVDs) are a leading cause of global mortality.
- Mitochondrial dysfunction is a key factor in CVD pathogenesis.
- Sirtuin 3 (SIRT3), a mitochondrial deacetylase, regulates mitochondrial function and oxidative stress.
Purpose of the Study:
- To evaluate the association between SIRT3 levels and CVDs.
- To elucidate SIRT3's role in CVD pathogenesis.
- To assess SIRT3's potential as a CVD biomarker.
Main Methods:
- Systematic literature search of MEDLINE and Embase databases (up to August 2024).
- Adherence to PRISMA guidelines for meta-analysis.
- Inclusion of observational studies comparing SIRT3 levels in CVD patients versus healthy controls.
Main Results:
- 8 studies with 397 participants were included.
- SIRT3 levels were significantly lower in individuals with CVDs (SMD: 1.08, p=0.0032).
- The most pronounced reduction in SIRT3 was observed in hypertension and dilated cardiomyopathy.
Conclusions:
- Compelling evidence shows significantly reduced SIRT3 levels in CVD patients.
- SIRT3 plays a critical role in cardiovascular diseases.
- SIRT3 holds potential as a biomarker and therapeutic target for CVDs.
Background:
Cardiovascular diseases (CVDs) remain the leading cause of mortality globally, with mitochondrial dysfunction playing a key role in their pathogenesis. SIRT3 (Sirtuin 3), a mitochondrial deacetylase, has emerged as a critical regulator of mitochondrial function and oxidative stress, with evidence linking its reduction to the progression of CVDs. This meta-analysis aimed to evaluate the association between SIRT3 levels and CVDs in order to elucidate its role in CVD pathogenesis and its potential as a biomarker.
Methods:
A systematic search of MEDLINE and Embase databases was conducted up to August 2024, adhering to PRISMA guidelines. Observational studies evaluating SIRT3 levels in human patients with CVDs as compared to healthy controls were included.
Results:
8 studies comprising 397 participants were included in this meta-analysis. Overall, SIRT3 levels were found to be significantly lower in individuals with CVDs compared to healthy controls (SMD: 1.08, 95% CI: 0.495-1.662, p = 0.0032). The reduction in SIRT3 levels was most pronounced in hypertension (SMD: 1.82) and dilated cardiomyopathy (SMD: 1.08).
Conclusion:
This meta-analysis provides compelling evidence of gsignificantly reduced SIRT3 levels in CVD patients, highlighting its critical role in cardiovascular diseases. These findings underscore the potential of SIRT3 as a biomarker and therapeutic target in CVDs.
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