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| http://dx.doi.org/10.1164/rccm.202207-1260LE | DOI Listing |
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SOCS domain targets ECM assembly in lung fibroblasts and experimental lung fibrosis.
Sci Rep
December 2024
Department of Chemistry and Biochemistry, Northern Arizona University, Flagstaff, AZ, USA.
Idiopathic pulmonary fibrosis (IPF) is a fatal disease defined by a progressive decline in lung function due to scarring and accumulation of extracellular matrix (ECM) proteins. The SOCS (Suppressor Of Cytokine Signaling) domain is a 40 amino acid conserved domain known to form a functional ubiquitin ligase complex targeting the Von Hippel Lindau (VHL) protein for proteasomal degradation. Here we show that the SOCS conserved domain operates as a molecular tool, to disrupt collagen and fibronectin fibrils in the ECM associated with fibrotic lung myofibroblasts.
View Article and Find Full Text PDFC3 deficiency promotes pulmonary inflammation in AT1R-induced mouse model for systemic sclerosis.
Front Immunol
December 2024
Priority Area Chronic Lung Diseases, Research Center Borstel - Leibniz Lung Center, Members of the German Center for Lung Research (DZL), Borstel, Germany.
Introduction: Autoantibody-mediated complement activation plays an essential role in a variety of autoimmune disorders. However, the role of complement in systemic sclerosis (SSc) remains largely unknown. In this study, we aimed to determine the role of complement C3 in the development of a recently described SSc mouse model based on autoimmunity to angiotensin II receptor type 1 (AT1R).
View Article and Find Full Text PDFThe immune mechanisms of acute exacerbations of idiopathic pulmonary fibrosis.
Front Immunol
December 2024
Department of Respiratory and Critical Medicine, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
Acute exacerbations of idiopathic pulmonary fibrosis (AE-IPF) are the leading cause of mortality among patients with IPF. There is still a lack of effective treatments for AE-IPF, resulting in a hospitalization mortality rate as high as 70%-80%. To reveal the complicated mechanism of AE-IPF, more attention has been paid to its disturbed immune environment, as patients with IPF exhibit deficiencies in pathogen defense due to local immune dysregulation.
View Article and Find Full Text PDFImpact of Janus kinase inhibitors and methotrexate on interstitial lung disease in rheumatoid arthritis patients.
Front Immunol
December 2024
Department of Immunology and Rheumatology, Division of Advanced Preventive Medical Sciences, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan.
Objectives: Little is known about how various treatments impact the progression of interstitial lung disease (ILD) in rheumatoid arthritis (RA) patients. Here, we compared ILD progression in RA patients treated with Janus kinase inhibitors (JAKi) or biological disease-modifying anti-rheumatic drugs (bDMARDs). experiments were also performed to evaluate the potential effects of the drugs on epithelial-mesenchymal transition (EMT), a key event in pulmonary fibrosis.
View Article and Find Full Text PDFInvestigates the Role of PANoptosis in Idiopathic Pulmonary Fibrosis and Potential Therapeutic Targets.
J Inflamm Res
December 2024
Department of Traumatology, Chongqing Emergency Medical Center, Chongqing University Central Hospital, Chongqing, 40014, People's Republic of China.
Purpose: Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive lung disease. PANoptosis, a unique inflammatory programmed cell death, it manifests as the simultaneous activation of signaling markers for pyroptosis, apoptosis, and necroptosis. However, research on the role of PANoptosis in the development of IPF is currently limited.
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