Abstract

Pathological cardiac hypertrophy is an important risk factor for cardiovascular disease. Ganoderic acid A (GAA), the primary bioactive constituent of Ganoderma lucidum ( G. lucidum ), is known for its stable chemical properties and diverse biological activities. It has been shown to confer protection against myocardial ischemia–reperfusion injury in rat models, potentially through modulating inflammatory responses and inhibiting protein expression linked to both NF-κB and apoptosis pathways. Nevertheless, the role of GAA in cardiac hypertrophy has not yet been fully elucidated. Using transverse aortic constriction (TAC)-induced cardiac hypertrophy in mice, we analyzed the degree of hypertrophy using echocardiography and at the pathology and molecular levels. Our results demonstrate that GAA effectively attenuates Ang II-induced cardiomyocyte hypertrophy in vitro and reduces pressure overload-induced cardiac hypertrophy in vivo. Further investigation revealed that GAA exerts its anti-hypertrophic effects by downregulating the mRNA expression of hypertrophic and fibrotic markers and attenuating inflammatory responses, and that the protective effects of GAA may involve NF-κB signaling. This study provides valuable theoretical support for the potential therapeutic application of GAA in treating pathological myocardial hypertrophy and heart failure.