<p>Cardiometabolic diseases (CMD) encompass a cluster of cardiovascular disorders primarily driven by metabolic dysregulation, such as obesity-associated cardiomyopathy, hypertensive heart disease, and diabetic cardiomyopathy. The pathogenesis of CMD is closely linked to chronic inflammation, myocardial hypertrophy, and mitochondrial energy metabolism dysfunction. Recently, the succinate-GPR91 pathway, a critical hub for metabolic regulation, has gained attention for its role in CMD. In addition to its function as an intermediate in the TCA cycle, succinate also exerts a range of pathophysiological effects by acting as a signaling molecule through the activation of its receptor, GPR91.Studies indicate that in metabolic disorders such as obesity, hypertension, diabetes,and atherosclerosis, abnormal activation of the succinate-GPR91 axis exacerbates inflammation, accelerates myocardial hypertrophy, and induces mitochondrial dysfunction, contributing to cardiovascular damage. Targeting the succinate-GPR91 pathway may offer novel CMD therapies. This article reviews succinate's role in inflammation, hypertrophy, mitochondrial dysfunction, and other diseases, offering insights for CMD research and treatment.</p> Graphical Abstract <p>The Succinate-GPR91 signaling axis plays a pivotal role in the development of cardiometabolic diseases (CMD) by amplifying inflammation, promoting myocardial hypertrophy, and disrupting mitochondrial energy metabolism. In metabolic disorders like obesity, hypertension, diabetes, and atherosclerosis, abnormal activation of this pathway exacerbates these pathological processes, ultimately contributing to cardiovascular damage. Targeting the succinate-GPR91 axis could provide novel therapeutic strategies for managing CMD and its associated complications.</p> <p></p>