Research Advances in the Mechanisms of Pannexin-1 Channels in Cardiovascular Diseases

Abstract

Cardiovascular diseases (CVDs), a leading global cause of mortality, are characterized by complex pathogenesis involving multifactorial molecular and cellular processes. Pannexin-1 (Panx1), a transmembrane channel protein, facilitates intercellular signaling through regulated release of small molecules such as adenosine triphosphate (ATP), thereby modulating diverse physiological and pathological pathways. This review explores the structural and functional landscape of Panx1, including its physiological roles, post-translational modifications and activation mechanisms. Its contributions to the pathophysiology of myocardial ischemia-reperfusion injury, cardiac remodeling, electrophysiological abnormalities, and diabetic cardiomyopathy are emphasized. Current evidence highlights the dual pathophysiological roles of Panx1 channels in CVDs: whereas ATP-mediated activation initiates cytoprotective signaling cascades, channel hyperactivation exacerbates pathological progression. Future research should prioritize mechanistic elucidation of Panx1’s molecular biology, and the development of targeted inhibitors with enhanced specificity and therapeutic efficacy, to advance novel therapeutic strategies for cardiovascular disorders.

Keywords

Cardiovascular Diseases (CVDs) / Pannexin-1 (Panx1) / Adenosine Triphosphate (ATP)

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