Caveolin-1-derived peptide attenuates cigarette smoke-induced airway and alveolar epithelial injury
Abstract
Chronic cigarette smoke (CS) exposure remains a major risk factor for the pathogenesis of COPD, a debilitating disease with no effective treatment. Increased caveolin-1 mediated induction of p53 and downstream plasminogen activator inhibitor-1 (PAI-1) expression contributes to CS-induced airway mucus hypersecretion and alveolar wall damage. This is reversed by caveolin-1 scaffolding domain peptide (CSP7) in preclinical models, suggesting the therapeutic potential of CSP7 for treating CS-induced lung injury (CS-LI) and COPD.
Document Details
- Document Type
- Pub Defense Publication
- Publication Date
- Nov 01, 2023
- Source ID
- 10.1152/ajplung.00178.2022
Entities
People
- Ashoka Kumar Bhagavath
- Bijesh Puthusseri
- Durgesh Nandini Das
- Gerald J. Criner
- Hua Tang
- Liang Fan
- Nagarjun V. Konduru
- Nathaniel Marchetti
- Sreerama Shetty
- Sudhir Bolla
- Venkadesaperumal Gopu
- Venugopal Krishnan
- Yogesh Saini
Organizations
- FAMRI
- Louisiana State University
- National Heart, Lung, and Blood Institute
- National Institute of Environmental Health Sciences
- Temple University
- University of Texas Health Science Center at Tyler