特发性肺纤维化
肌成纤维细胞
代谢组学
肺纤维化
肺
纤维化
囊性纤维化
病理
医学
生物
癌症研究
内科学
生物信息学
作者
Willy Roque,Freddy Romero
出处
期刊:American Journal of Physiology-cell Physiology
[American Physiological Society]
日期:2021-05-01
卷期号:320 (5): C689-C695
被引量:37
标识
DOI:10.1152/ajpcell.00586.2020
摘要
Idiopathic pulmonary fibrosis (IPF) is a chronic and progressive lung disease of unknown etiology with limited treatment options. It is characterized by repetitive injury to alveolar epithelial cells and aberrant activation of numerous signaling pathways. Recent evidence suggests that metabolic reprogramming, metabolic dysregulation, and mitochondria dysfunction are distinctive features of the IPF lungs. Through numerous mechanisms, metabolomic abnormalities in alveolar epithelial cells, myofibroblast, macrophages, and fibroblasts contribute to the abnormal collagen synthesis and dysregulated airway remodeling described in lung fibrosis. This review summarizes the metabolomic changes in amino acids, lipids, glucose, and heme seen in IPF lungs. Simultaneously, we provide new insights into potential therapeutic strategies by targeting a variety of metabolites.
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