Pharmacological modulation of TRP channels emerges as a promising therapeutic strategy for cardiac hypertrophy by targeting calcium homeostasis, apoptosis, and fibrosis.
TRP channels represent a promising emerging therapeutic target for the precision management of cardiac hypertrophy.
INTRODUCTION Cardiac hypertrophy (CH) is a major contributor to cardiovascular disease (CVD), affecting millions worldwide. While initially an adaptive response, sustained hypertrophic stimuli lead to maladaptive outcomes, including heart failure (HF), contractile dysfunction, and ventricular remodeling. Key pathophysiological processes involve myocardial fibrosis, cardiomyocyte death, mitochondrial impairment and Ca2+ dysregulation. Despite available therapies, treatment of CH is symptomatic with no approved targeted options. Many interventions have only temporary benefits, may cause adverse hemodynamic effects, and involve procedural risks.AREAS COVERED This review highlights TRP channels as emerging therapeutic targets in CH. TRP channels play pivotal roles in calcium (Ca2+) homeostasis and modulate apoptosis, cell proliferation, hypoxia adaptation, inflammation, and metabolic reprogramming, core drivers of cardiac remodeling. Pharmacological modulation of TRP activity may counter pathological hypertrophy by tuning hypertrophic signaling, mitigating fibrosis, and enhancing cardiac performance. Incorporating TRP-targeted strategies into treatment paradigms could help address the limitations of current therapies.EXPERT OPINION We propose that TRP channel-based interventions with mechanistic insights, hold significant promise for precision management of CH. Many TRP subtypes remain uncharacterized, and their investigation could reveal new therapeutic aspects. Future research should prioritize mapping TRP-mediated pathways and validating their translational potential.
Upadhyay et al. (Thu,) conducted a review in Cardiac hypertrophy. Pharmacological modulation of TRP channels was evaluated. Pharmacological modulation of TRP channels emerges as a promising therapeutic strategy for cardiac hypertrophy by targeting calcium homeostasis, apoptosis, and fibrosis.