Aging Delays Lung Repair: Insights from Omics Analysis in Mice with Pulmonary Fibrosis
Author:
Affiliation:
1. Department of Medicine and Women’s Guild Lung InstituteCedars-Sinai Medical CenterLos Angeles, California
2. Department of MedicineBoston University School of MedicineBoston, Massachusetts
Publisher
American Thoracic Society
Subject
Cell Biology,Clinical Biochemistry,Pulmonary and Respiratory Medicine,Molecular Biology
Link
https://www.atsjournals.org/doi/pdf/10.1165/rcmb.2023-0171ED
Reference15 articles.
1. Hyaluronan and TLR4 promote surfactant-protein-C-positive alveolar progenitor cell renewal and prevent severe pulmonary fibrosis in mice
2. Targeted Injury of Type II Alveolar Epithelial Cells Induces Pulmonary Fibrosis
3. Lung Fibroblasts, Aging, and Idiopathic Pulmonary Fibrosis
4. The ZIP8/SIRT1 axis regulates alveolar progenitor cell renewal in aging and idiopathic pulmonary fibrosis
5. Serpine 1 induces alveolar type II cell senescence through activating p53-p21-Rb pathway in fibrotic lung disease
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1. Aging-Associated Metabolite Methylmalonic Acid Increases Susceptibility to Pulmonary Fibrosis;The American Journal of Pathology;2024-08
2. Lipid Deficiency Contributes to Impaired Alveolar Progenitor Cell Function in Aging and Idiopathic Pulmonary Fibrosis;American Journal of Respiratory Cell and Molecular Biology;2024-08
3. Environmental tobacco smoke exposure exaggerates bleomycin-induced collagen overexpression during pulmonary fibrogenesis;Journal of Inflammation;2024-03-20
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