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Published on: February 4, 2021
The Role of Adiponectin and Leptin in Fibro-Calcific Aortic Valve Disease: A Systematic Review and Meta-Analysis
Veronika A Myasoedova1, Francesca Bertolini1, Vincenza Valerio1
1Centro Cardiologico Monzino IRCCS, 20138 Milan, Italy.
Insights
This meta-analysis suggests elevated leptin levels may be linked to severe aortic stenosis, while adiponectin
Area of Science:
- Cardiology
- Biochemistry
- Genetics
Background:
- Fibro-calcific aortic valve disease (FCAVD) is a progressive condition leading to aortic stenosis.
- The roles of adiponectin and leptin in cardiovascular diseases are debated, with unclear links to FCAVD.
- This study investigates adiponectin and leptin in FCAVD, focusing on severe aortic stenosis (AS).
Purpose of the Study:
- To evaluate the association between adiponectin and leptin levels and FCAVD.
- To specifically examine these associations in patients with severe aortic stenosis.
- To clarify the potential role of these adipokines in FCAVD pathogenesis.
Main Methods:
- A systematic literature search was performed across PubMed, Scopus, and Web of Science.
- Ten studies with 2360 participants (989 FCAVD, 1371 controls) were included.
- Standardized mean differences (SMDs) and 95% confidence intervals (CIs) were calculated.
Main Results:
- A trend suggested lower adiponectin levels (SMD = -0.143) and higher leptin levels (SMD = 0.175) in FCAVD.
- Low adiponectin remained a trend, but high leptin showed a significant correlation with severe AS (SMD = 0.29, p = 0.025).
- Publication bias was assessed using Egger's test and funnel plots.
Conclusions:
- Elevated leptin levels show a potential association with severe aortic stenosis.
- The relationship between adiponectin and FCAVD requires further investigation.
- These adipokines may serve as biomarkers for FCAVD progression, warranting more research.
Background:
Fibro-calcific aortic valve disease (FCAVD) is a progressive disorder characterized by the thickening and calcification of the aortic valve, eventually leading to aortic stenosis. Adiponectin and leptin, known for their anti-inflammatory and proinflammatory properties, respectively, have been implicated in cardiovascular diseases, but their associations with FCAVD are controversial. This meta-analysis aims to evaluate the relationships between adiponectin and leptin levels and FCAVD, particularly in patients with severe aortic stenosis (AS).
Methods:
A systematic search was conducted across the PubMed, Scopus, and Web of Science databases to identify studies on adiponectin and leptin levels in FCAVD. The methodological quality of each study was assessed using the Newcastle-Ottawa Scale. Standardized mean differences (SMDs) and 95% confidence intervals (CIs) were calculated, and publication bias was evaluated using Egger's test and funnel plots.
Results:
Out of 191 articles identified, 10 studies involving 2360 patients (989 with FCAVD and 1371 controls) were included. The analysis suggested trends in the associations of lower adiponectin levels (SMD = -0.143, 95% CI: -0.344, 0.057, p = 0.161) and higher leptin levels (SMD = 0.175, 95% CI: -0.045, 0.395, p = 0.119) with FCAVD. The association remained a trend for low adiponectin but showed a significant correlation with high leptin in severe AS patients (SMD = 0.29, 95% CI: 0.036, 0.543, p = 0.025).
Conclusion:
This meta-analysis indicates a potential association between elevated leptin levels and severe aortic stenosis, while the relationship with adiponectin levels remains inconclusive. These findings highlight the need for further and dedicated research to clarify the roles of these adipokines in the pathogenesis of FCAVD and their potential roles as biomarkers for disease progression.

