Idiopathic Pulmonary Fibrosis Caused by Damaged Mitochondria and Imbalanced Protein Homeostasis in Alveolar Epithelial Type II Cell.

Autor: Dong Z; Affiliated Cancer Hospital & Institute of Guangzhou Medical University, State Key Laboratory of Respiratory Disease, School of Biomedical Engineering, Guangzhou Medical University, Guangzhou, 510260, China.; Institute of Biophysics, Chinese Academy of Sciences 15 Datun Road, Chaoyang District, Beijing, 100101, China.; College of Life Science, Mudanjiang Medical University, Mudanjiang, 157000, China., Wang X; Affiliated Cancer Hospital & Institute of Guangzhou Medical University, State Key Laboratory of Respiratory Disease, School of Biomedical Engineering, Guangzhou Medical University, Guangzhou, 510260, China., Wang P; College of Life Science, Mudanjiang Medical University, Mudanjiang, 157000, China., Bai M; Affiliated Cancer Hospital & Institute of Guangzhou Medical University, State Key Laboratory of Respiratory Disease, School of Biomedical Engineering, Guangzhou Medical University, Guangzhou, 510260, China.; School of Chemistry and Biological Engineering, University of Science and Technology Beijing, Beijing, 100101, China., Wang T; School of Chemistry and Biological Engineering, University of Science and Technology Beijing, Beijing, 100101, China., Chu Y; College of Life Science, Mudanjiang Medical University, Mudanjiang, 157000, China., Qin Y; Affiliated Cancer Hospital & Institute of Guangzhou Medical University, State Key Laboratory of Respiratory Disease, School of Biomedical Engineering, Guangzhou Medical University, Guangzhou, 510260, China.; Institute of Biophysics, Chinese Academy of Sciences 15 Datun Road, Chaoyang District, Beijing, 100101, China.
Jazyk: angličtina
Zdroj: Advanced biology [Adv Biol (Weinh)] 2024 Oct 10, pp. e2400297. Date of Electronic Publication: 2024 Oct 10.
DOI: 10.1002/adbi.202400297
Abstrakt: Alveolar epithelial Type II (ATII) cells are closely associated with early events of Idiopathic pulmonary fibrosis (IPF). Proteostasis dysfunction, endoplasmic reticulum (ER) stress, and mitochondrial dysfunction are known causes of decreased proliferation of alveolar epithelial cells and the secretion of pro-fibrotic mediators. Here, a large body of evidence is systematized and a cascade relationship between protein homeostasis, endoplasmic reticulum stress, mitochondrial dysfunction, and fibrotropic cytokines is proposed, providing a theoretical basis for ATII cells dysfunction as a possible pathophysiological initiating event for idiopathic pulmonary fibrosis.
(© 2024 The Author(s). Advanced Biology published by Wiley‐VCH GmbH.)
Databáze: MEDLINE
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