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• W3122823671 endingPage "274" @default.
• W3122823671 startingPage "261" @default.
• W3122823671 abstract "Abstract There have been recent extensive studies and rapid advancement on the pathogenesis underlying idiopathic pulmonary fibrosis (IPF), and intricate pathogenesis of IPF has been suggested. The purpose of this study was to clarify the logical relationship between these mechanisms. An extensive search was undertaken of the PubMed using the following keywords: “etiology,” “pathogenesis,” “alveolar epithelial cell (AEC),” “fibroblast,” “lymphocyte,” “macrophage,” “epigenomics,” “histone,” acetylation,” “methylation,” “endoplasmic reticulum stress,” “mitochondrial dysfunction,” “telomerase,” “proteases,” “plasminogen,” “epithelial-mesenchymal transition,” “oxidative stress,” “inflammation,” “apoptosis,” and “idiopathic pulmonary fibrosis.” This search covered relevant research articles published up to April 30, 2020. Original articles, reviews, and other articles were searched and reviewed for content; 240 highly relevant studies were obtained after screening. IPF is likely the result of complex interactions between environmental, genetic, and epigenetic factors: environmental exposures affect epigenetic marks; epigenetic processes translate environmental exposures into the regulation of chromatin; epigenetic processes shape gene expression profiles; in turn, an individual's genetic background determines epigenetic marks; finally, these genetic and epigenetic factors act in concert to dysregulate gene expression in IPF lung tissue. The pathogenesis of IPF involves various imbalances including endoplasmic reticulum, telomere length homeostasis, mitochondrial dysfunction, oxidant/antioxidant imbalance, Th1/Th2 imbalance, M1–M2 polarization of macrophages, protease/antiprotease imbalance, and plasminogen activation/inhibition imbalance. These affect each other, promote each other, and ultimately promote AEC/fibroblast apoptosis imbalance directly or indirectly. Excessive AEC apoptosis and impaired apoptosis of fibroblasts contribute to fibrosis. IPF is likely the result of complex interactions between environmental, genetic, and epigenetic factors. The pathogenesis of IPF involves various imbalances centered on AEC/fibroblast apoptosis imbalance." @default.
• W3122823671 created "2021-02-01" @default.
• W3122823671 creator A5004282357 @default.
• W3122823671 creator A5024648164 @default.
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• W3122823671 creator A5070011390 @default.
• W3122823671 creator A5072315367 @default.
• W3122823671 creator A5080435070 @default.
• W3122823671 date "2021-01-14" @default.
• W3122823671 modified "2023-10-18" @default.
• W3122823671 title "Role of various imbalances centered on alveolar epithelial cell/fibroblast apoptosis imbalance in the pathogenesis of idiopathic pulmonary fibrosis" @default.
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