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- W4385275411 endingPage "102183" @default.
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- W4385275411 abstract "The incidence of pulmonary fibrosis is on the rise, and existing treatments have limited efficacy in improving patient survival. The purpose of this study was to reveal the potential of Krüppel-like factor (KLF)15 activation in alleviating pulmonary fibrosis. Transforming growth factor beta (TGF-β) was utilized to induce lung fibroblasts to establish an in vitro model of pulmonary fibrosis. The impacts of TGF-β and KLF15 level on cell proliferation, migration, extracellular matrix (ECM) accumulation, and endoplasmic reticulum stress (ERS) were assessed. Additionally, tunicamycin, an ERS agonist, was used to investigate the role of ERS in KLF15 regulation. The results showed that KLF15 was dropped in response to TGF-β treatment. However, KLF15 overexpression reduced cell proliferation, migration, ECM accumulation, and ERS, alleviating the effects of TGF-β stimulation. Subsequent treatment with tunicamycin diminished the effects of KLF15 overexpression, demonstrating that ERS mediated the modulation of KLF15. KLF15 acts against ERS and suppresses excessive proliferation and ECM accumulation in lung fibroblast. These findings suggest that activating KLF15 is a promising strategy for alleviating pulmonary fibrosis." @default.
- W4385275411 created "2023-07-27" @default.
- W4385275411 creator A5006667929 @default.
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- W4385275411 date "2023-10-01" @default.
- W4385275411 modified "2023-09-27" @default.
- W4385275411 title "Krüppel-like factor 15 counteracts endoplasmic reticulum stress and suppresses lung fibroblast proliferation and extracellular matrix accumulation" @default.
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- W4385275411 doi "https://doi.org/10.1016/j.tice.2023.102183" @default.
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