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WSB1, a Hypoxia-Inducible E3 Ligase, Promotes Myofibroblast Accumulation and Attenuates Alveolar Epithelial Regeneration in Mouse Lung Fibrosis. | LitMetric

AI Article Synopsis

  • Idiopathic pulmonary fibrosis (IPF) is a serious lung disease with no cure, characterized by ongoing lung damage, myofibroblast buildup, and excessive collagen leading to poor oxygen levels and respiratory failure.* -
  • The study focused on WSB1, an E3 ubiquitin ligase that is significantly linked to hypoxia, showing that its expression increased with lung injury in mice, indicating its involvement in the progression of fibrosis.* -
  • Deleting Wsb1 in adult mice reduced lung fibrosis and improved lung cell recovery, suggesting that targeting WSB1 could be a promising approach for treating pulmonary fibrosis.*

Article Abstract

Idiopathic pulmonary fibrosis is a progressive interstitial lung disease for which there is no curative therapy available. Repetitive alveolar epithelial injury repair, myofibroblast accumulation, and excessive collagen deposition are key pathologic features of idiopathic pulmonary fibrosis, eventually leading to cellular hypoxia and respiratory failure. The precise mechanism driving this complex maladaptive process remains inadequately understood. WD repeat and suppressor of cytokine signaling box containing 1 (WSB1) is an E3 ubiquitin ligase, the expression of which is associated strongly with hypoxia, and forms a positive feedback loop with hypoxia-inducible factor 1α (HIF-1α) under anoxic condition. This study explored the expression, cellular distribution, and function of WSB1 in bleomycin (BLM)-induced mouse lung injury and fibrosis. WSB1 expression was highly induced by BLM injury and correlated with the progression of lung fibrosis. Significantly, conditional deletion of Wsb1 in adult mice ameliorated BLM-induced pulmonary fibrosis. Phenotypically, Wsb1-deficient mice showed reduced lipofibroblast to myofibroblast transition, but enhanced alveolar type 2 proliferation and differentiation into alveolar type 1 after BLM injury. Proteomic analysis of mouse lung tissues identified caveolin 2 as a potential downstream target of WSB1, contributing to BLM-induced epithelial injury repair and fibrosis. These findings unravel a vital role for WSB1 induction in lung injury repair, thus highlighting it as a potential therapeutic target for pulmonary fibrosis.

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Source
http://dx.doi.org/10.1016/j.ajpath.2024.01.010DOI Listing

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