Oxidative and Endoplasmic Reticulum (ER) Stress in Tissue Fibrosis

Abstract

Various extrinsic stresses, including hypoxia and oxidative stress, trigger the progression of diseases associated with inflammation and fibrosis via the pathogenic alteration of these stress signals.They include the HIF pathway, induced by hypoxia, and the Nrf2 pathway, induced by oxidative stress. Recent evidence emphasizes that the extrinsic stress-induced phenotypic changes are widely associated with endoplasmic reticulum (ER) stress and induction of the ER stress signal, unfolded protein response. This issue focuses on the recent insights demonstrating the link between molecular mechanisms leading to fibrosis and stress signals. In particular, we summarized the contribution of hypoxia, oxidative stress, and ER stress signals, all of which are common pathogenic pathways for the progression of chronic renal disease, to fibrotic changes, as well as the future aspects of therapeutic approaches targeting these stress pathways to fibrosis in various organs.