Caveolin-1 as a critical component in the pathogenesis of lung fibrosis of different etiology: Evidences and mechanisms
Abstract
Caveolin is a structural protein of flask-shaped invaginations of the plasma membrane termed as caveolae and is widely expressed on the endothelial cells, smooth muscle cells and fibroblasts in the different parts of the body including the lung tissues. The expression of caveolin-1 in the lung tissues is important to prevent the fibrogenic actions of TGF-β1 in lung fibrosis of different etiology including idiopathic pulmonary fibrosis, systemic sclerosis-associated interstitial lung disease and allergen-induced airway remodeling. Caveolin-1-mediated internalization and degradation of TGF-β1 receptors may possibly account for the decreased actions of TGF-β1. Studies have shown that the deficiency of caveolin-1 is very important in inducing lung fibrosis and its upregulation is reported to prevent lung fibrosis. The biological actions of caveolin-1 involve signaling pathways including JNK signaling, IL-4, STAT-3, miR199a-5p, CXCR4 + and CXCL12. The present review discusses the key role of caveolin and associated signaling pathways in the pathogenesis of lung fibrosis of different etiology.
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Caveolin-1 protein is a structural protein that plays a critical role in regulating lung repair and cellular movement by restoring pathways that both promote epithelial health and halt fibrosis in the lung.
“Caveolin-1 protein (Cav-1) is a structural protein that plays a critical role in regulating lung repair and cellular movement by restoring pathways that both promote epithelial health and halt fibrosis in the lung7–9.”
From Inhaled LTI-03 for idiopathic pulmonary fibrosis: a randomized dose escalation study (2026) · cites this paper as [8]
Cites
Sanders, Y. Y., Cui, Z., Le Saux, C. J., Horowitz, J. C., Rangarajan, S., Kurundkar, A., Antony, V. B., & Thannickal, V. J. (2015) · PLOS ONE · doi:10.1371/journal.pone.0116995 · Cited by 49 · see citing works
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LTI-03 peptide demonstrates anti-fibrotic activity in ex vivo lung slices from patients with IPF
MacKenzie, B., Mahavadi, P., Pinho Jannini-Sa, Y. A., Creyns, B., Coelho, A. L., Espindola, M., Ruppert, C., Windsor, B., Aigner, C., Hogaboam, C. M., et al. (2025) · iScience · doi:10.1016/j.isci.2025.113437 · Cited by 2 · see citing works
Inhaled LTI-03 for idiopathic pulmonary fibrosis: a randomized dose escalation study
Molyneaux, P. L., Hirani, N. A., Chia, C. C. K., Kulkarni, T., Zaman, T., Kaner, R. J., Coelho, A. L., Jannini-Sa, Y. A. P., Windsor, B., Kruger, S., et al. (2026) · Nature Communications · doi:10.1038/s41467-026-75291-3 · Cited by 1 · see citing works
- Authors
- Kulshrestha, R., Singh, H., Pandey, A., Mehta, A., Bhardwaj, S., & Jaggi, A. S.
- Affiliations
- University of Delhi (IN)
- Punjabi University (IN)
- Corresponding author
- Jaggi, Amteshwar Singh
- Venue
- Experimental and Molecular Pathology
- Publisher
- Elsevier BV
- Published
- 2019-12
- Volume
- 111
- Pages
- 104315
- ISSN
- 0014-4800 (ISSN-L)
- OpenAlex
- W2980626003
- Cited by
- 19
- References
- 1
- Citations by year
- 2026: 3 · 2025: 4 · 2024: 4 · 2022: 3 · 2021: 3 · 2020: 2
- FWCI
- 0.23
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Experimental and Molecular Pathology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Caveolin-1 and cellular processes
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
- Health Sciences › Medicine › Pathology and Forensic Medicine › Systemic Sclerosis and Related Diseases
- Keywords
- caveolin-1, pulmonary fibrosis, idiopathic pulmonary fibrosis, systemic sclerosis-associated interstitial lung disease, TGF-β1 signaling, caveolae, JNK signaling, STAT3, IL-4, miR-199a-5p, fibrosis pathogenesis
- MeSH terms
- Animals, Humans, Pulmonary Fibrosis, Signal Transduction, Cytokines, Epigenesis, Genetic, JNK Mitogen-Activated Protein Kinases, STAT Transcription Factors, Caveolin 1, Idiopathic Pulmonary Fibrosis, Airway Remodeling
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