The critical roles of caveolin-1 in lung diseases
Open accessAbstract
Caveolin-1 (Cav-1), a structural and functional component in the caveolae, plays a critical role in transcytosis, endocytosis, and signal transduction. Cav-1 has been implicated in the mediation of cellular processes by interacting with a variety of signaling molecules. Cav-1 is widely expressed in the endothelial cells, smooth muscle cells, and fibroblasts in the various organs, including the lungs. The Cav-1-mediated internalization and regulation of signaling molecules participate in the physiological and pathological processes. Particularly, the MAPK, NF-κB, TGFβ/Smad, and eNOS/NO signaling pathways have been involved in the regulatory effects of Cav-1 in lung diseases. The important effects of Cav-1 on the lungs indicate that Cav-1 can be a potential target for the treatment of lung diseases. A Cav-1 scaffolding domain peptide CSP7 targeting Cav-1 has been developed. In this article, we mainly discuss the structure of Cav-1 and its critical roles in lung diseases, such as pneumonia, acute lung injury (ALI), asthma, chronic obstructive pulmonary disease (COPD), pulmonary hypertension, pulmonary fibrosis, and lung cancer.
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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 [9]
The Introduction describes Cav-1 as a structural component of caveolae involved in cell migration. Section 4.5 (Pulmonary fibrosis) reports that Cav-1-derived peptides inhibit alveolar epithelial-cell apoptosis and attenuate experimental fibrosis, but it attributes restoration of p53 expression specifically to CSP7; it does not say Cav-1 itself restores pathways that halt lung fibrosis. (LLM, conf=0.86)
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CAV1 is a prognostic predictor for patients with idiopathic pulmonary fibrosis and lung cancer
Yin, D., Qiu, J., Hu, S., Cheng, L., Li, H., Cheng, X., Wang, S., & Lü, J. (2022) · Journal of Biosciences · doi:10.1007/s12038-021-00245-4 · Cited by 13 · see citing works
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Caveolin-1-derived peptide attenuates cigarette smoke-induced airway and alveolar epithelial injury
Das, D. N., Puthusseri, B., Gopu, V., Krishnan, V., Bhagavath, A. K., Bolla, S., Saini, Y., Criner, G. J., Marchetti, N. T., Tang, H., et al. (2023) · American Journal of Physiology-Lung Cellular and Molecular Physiology · doi:10.1152/ajplung.00178.2022 · Cited by 12 · see citing works
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- Authors
- Fan, J., Zheng, S., Wang, M., & Yuan, X.
- Affiliations
- First Affiliated Hospital of Gannan Medical University (CN)
- Corresponding author
- Yuan, Xiaoliang
- Venue
- Frontiers in Pharmacology
- Publisher
- Frontiers Media SA
- Published
- 2024-09-24
- Volume
- 15
- Pages
- 1417834-1417834
- ISSN
- 1663-9812 (ISSN-L)
- PMC
- PMC11458383
- OpenAlex
- W4402753012
- Cited by
- 21
- References
- 218
- Citations by year
- 2026: 14 · 2025: 6 · 2024: 1
- FWCI
- 1.11
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Frontiers in Pharmacology (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Caveolin-1 and cellular processes
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Angiogenesis and VEGF in Cancer
- Health Sciences › Medicine › Pharmacology › Flavonoids in Medical Research
- Keywords
- caveolin-1, caveolae, lung disease, MAPK signaling, NF-κB signaling, TGF-β/Smad signaling, pneumonia, acute lung injury, asthma, chronic obstructive pulmonary disease, pulmonary hypertension, pulmonary fibrosis, lung cancer
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