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Ganoderic Acid A Attenuates Pathological Cardiac Hypertrophy by Attenuating Inflammatory Responses.
Changlin Zhen1,2, Yonghui Zhang1,2, Hui Tan1,2
1School of Basic Medical Sciences, Chongqing Three Gorges Medical College, Chongqing 404120, China.
Current Issues in Molecular Biology
|May 27, 2026
Summary
Ganoderic acid A (GAA) from Ganoderma lucidum effectively treats cardiac hypertrophy by reducing inflammation and NF-κB signaling. This finding supports GAA as a potential therapy for heart failure.
Area of Science:
- Cardiovascular Research
- Pharmacology
- Integrative Medicine
Background:
- Pathological cardiac hypertrophy is a major risk factor for cardiovascular disease.
- Ganoderic acid A (GAA), from Ganoderma lucidum, has known protective effects against myocardial ischemia-reperfusion injury.
- The role of GAA in cardiac hypertrophy remains largely unelucidated.
Purpose of the Study:
- To investigate the therapeutic potential of Ganoderic acid A (GAA) in mitigating cardiac hypertrophy.
- To elucidate the molecular mechanisms underlying GAA's anti-hypertrophic effects.
Main Methods:
- Cardiac hypertrophy was induced in mice using transverse aortic constriction (TAC).
- In vitro studies assessed Ang II-induced cardiomyocyte hypertrophy.
- Echocardiography, pathological, and molecular analyses were performed.
Main Results:
- GAA significantly attenuated Ang II-induced cardiomyocyte hypertrophy in vitro.
- GAA reduced pressure overload-induced cardiac hypertrophy in vivo.
- GAA downregulated hypertrophic/fibrotic markers and inflammatory responses, potentially via NF-κB signaling.
Conclusions:
- GAA demonstrates significant efficacy in treating pathological cardiac hypertrophy.
- GAA's protective effects involve the downregulation of hypertrophic, fibrotic, and inflammatory pathways, including NF-κB signaling.
- GAA shows promise as a therapeutic agent for pathological myocardial hypertrophy and heart failure.
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