TRP channels in cardiac and intestinal fibrosis.

Semin Cell Dev Biol

Department of Physiology, Fukuoka University School of medicine, Nanakuma 7-451, Jonan-ku, Fukuoka 814-0180, Japan.

Published: October 2019

AI Article Synopsis

  • Advanced fibrosis is a significant factor in many chronic inflammatory disorders, contributing to high rates of illness and death in today's society.
  • Research highlights the important roles of transient receptor potential (TRP) channels in the mechanisms of advanced fibrosis, suggesting that they may influence inflammatory processes in various organs.
  • The paper specifically discusses the link between TRP channels and fibrosis in the heart and intestines, emphasizing their relevance to conditions like atrial fibrillation and Crohn's disease.

Article Abstract

It is now widely accepted that advanced fibrosis underlies many chronic inflammatory disorders and is the main cause of morbidity and mortality of the modern world. The pathogenic mechanism of advanced fibrosis involves diverse and intricate interplays between numerous extracellular and intracellular signaling molecules, among which the non-trivial roles of a stress-responsive Ca/Na-permeable cation channel superfamily, the transient receptor potential (TRP) protein, are receiving growing attention. Available evidence suggests that several TRP channels such as TRPC3, TRPC6, TRPV1, TRPV3, TRPV4, TRPA1, TRPM6 and TRPM7 may play central roles in the progression and/or prevention of fibroproliferative disorders in vital visceral organs such as lung, heart, liver, kidney, and bowel as well as brain, blood vessels and skin, and may contribute to both acute and chronic inflammatory processes involved therein. This short paper overviews the current knowledge accumulated in this rapidly growing field, with particular focus on cardiac and intestinal fibrosis, which are tightly associated with the pathogenesis of atrial fibrillation and inflammatory bowel diseases such as Crohn's disease.

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http://dx.doi.org/10.1016/j.semcdb.2018.11.002DOI Listing

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