From oxidative stress to metabolic dysfunction: The role of TRPM2

Abstract

Metabolic syndromes including atherosclerosis, diabetes, obesity, and hypertension are increasingly prevalent worldwide. The disorders are the primary attributes of oxidative stress and inflammation. The transient receptor potential M2 (TRPM2) channel is a pivotal mediator linking oxidative stress to metabolic dysfunction. TRPM2, a non-selective cation channel activated by reactive oxygen species (ROS) and adenosine diphosphate ribose (ADPR), regulates calcium influx, inflammation, and cell death across various tissues. This review explores the structural and activation mechanisms of TRPM2, emphasizing its significance in metabolic diseases. Elevated levels of TRPM2 play a vital role in the disease progression by influencing physiological and cellular processes such as endothelial dysfunction, immune cell activation, and mitochondrial impairment. In conditions such as atherosclerosis, ischemic stroke, diabetes, obesity, and hypertension; TRPM2 exacerbates oxidative damage, amplifies inflammatory responses, and disrupts metabolic homeostasis. Recent research highlights the potential of TRPM2 as a therapeutic target, developing specified inhibitors. This review underscores the multifaceted role of TRPM2 in metabolic disorders and its promise as a target for therapeutic interventions.

Keywords: Metabolic dysfunction; Oxidative stress; The transient receptor potential M2.