Cited by 22Caveolin-1 and cellular processesAngiogenesis and VEGF in CancerFlavonoids in Medical Research

The critical roles of caveolin-1 in lung diseases

Open access
Fan, Jiarun, Zheng, Siping, Wang, Maoping, Yuan, Xiaoliang·2024·Frontiers in Pharmacology

Abstract

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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Crossref · 10.3389/fphar.2024.1417834

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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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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
Published
2024-09-24
Volume
15
Pages
1417834-1417834
ISSN
1663-9812 (ISSN-L)
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
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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