Short Introduction for Fibrosis in Cardiovascular Diseases

Abstract

Fibrosis occurs in all organs and tissues except the brain, and its progression leads to dysfunction of affected organs. Fibrosis-induced organ dysfunction results from the loss of elasticity, strength, and functionality of tissues due to the extracellular matrix secreted by myofibroblasts that express smooth muscle-type actin as a marker. Myofibroblasts, which play a major role in fibrosis, were once thought to originate exclusively from activated fibroblasts; however, it is now clear that myofibroblasts are diverse in origin, from epithelial cells, endothelial cells, adipocytes, macrophages, and other cells. Fibrosis in the cardiovascular systems, such as the kidneys, heart, and lungs, is a serious chronic disease that ultimately leads to death. Indeed, fibrotic diseases are an important cause of morbidity and mortality worldwide and are responsible for up to 45% of all deaths in developed countries. This symposium will introduce the latest topics on the therapeutic strategies against fibrosis in the heart, kidneys, and lungs from basic research to clinical practice. We hope that this symposium will lead to the development of novel therapeutic strategies against tissue fibrosis.