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Evidence for a lipofibroblast-to- + myofibroblast reversible switch during the development and resolution of lung fibrosis in young mice.
Eur Respir J
November 2024
The Quzhou Affiliated Hospital of Wenzhou Medical University, Quzhou People's Hospital, Quzhou, Zhejiang, China.
Article Synopsis
- Fibrosis, especially idiopathic pulmonary fibrosis (IPF), is linked to abnormal healing processes in the lungs that can lead to organ failure, with no current cure.
- The study investigates activated myofibroblasts (aMYFs), their different subtypes, and their roles in lung repair and damage using genetic and transcriptomic analysis in mice, as well as human data.
- Findings reveal that aMYFs can be categorized into four distinct groups, with a specific subset linked to both the progression and resolution of fibrosis, suggesting new potential treatment targets for managing IPF.
Highlighting fibroblast plasticity in lung fibrosis: the WI-38 cell line as a model for investigating the myofibroblast and lipofibroblast switch.
Theranostics
July 2024
Cardio-Pulmonary Institute and Department of Pulmonary and Critical Care Medicine and Infectious Diseases, Universities of Giessen and Marburg Lung Center (UGMLC), member of the German Center for Lung Research (DZL), Justus-Liebig University Giessen, Giessen, Germany.
Myofibroblasts (MYFs) are generally considered the principal culprits in excessive extracellular matrix deposition and scar formation in the pathogenesis of lung fibrosis. Lipofibroblasts (LIFs), on the other hand, are defined by their lipid-storing capacity and are predominantly found in the alveolar regions of the lung. They have been proposed to play a protective role in lung fibrosis.
View Article and Find Full Text PDFWSB1, a Hypoxia-Inducible E3 Ligase, Promotes Myofibroblast Accumulation and Attenuates Alveolar Epithelial Regeneration in Mouse Lung Fibrosis.
Am J Pathol
May 2024
Medical Research Center, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China; Department of Pulmonary and Critical Care Medicine, The First Affiliated Hospital of Wenzhou Medical University, and Zhejiang Provincial Key Laboratory of Interventional Pulmonology, Wenzhou, China. Electronic address:
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.
View Article and Find Full Text PDFOmentin-1 induces mechanically activated fibroblasts lipogenic differentiation through pkm2/yap/pparγ pathway to promote lung fibrosis resolution.
Cell Mol Life Sci
September 2023
Department of Physiology, Xiangya School of Medicine, Central South University, Changsha, 410008, Hunan, China.
Idiopathic pulmonary fibrosis (IPF) is a progressive and fatal lung disease characterized by extensive extracellular matrix (ECM) deposition by activated myofibroblasts, which are specialized hyper-contractile cells that promote ECM remodeling and matrix stiffening. New insights on therapeutic strategies aimed at reversing fibrosis by targeting myofibroblast fate are showing promise in promoting fibrosis resolution. Previously, we showed that a novel adipocytokine, omentin-1, attenuated bleomycin (BLM)-induced lung fibrosis by reducing the number of myofibroblasts.
View Article and Find Full Text PDFComplex urban atmosphere alters alveolar stem cells niche properties and drives lung fibrosis.
Am J Physiol Lung Cell Mol Physiol
October 2023
Université Paris Est Créteil, INSERM, IMRB, FHU Senec, Créteil, France.
There is growing evidence suggesting that urban pollution has adverse effects on lung health. However, how urban pollution affects alveolar mesenchymal and epithelial stem cell niches remains unknown. This study aimed to determine how complex representative urban atmospheres alter alveolar stem cell niche properties.
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