» Articles » PMID: 37998001

Caveolin-1: A Review of Intracellular Functions, Tissue-Specific Roles, and Epithelial Tight Junction Regulation

Overview
Journal Biology (Basel)
Publisher MDPI
Specialty Biology
Date 2023 Nov 24
PMID 37998001
Authors
Affiliations
Soon will be listed here.
Abstract

Caveolin-1 (Cav1) is a vital protein for many cellular processes and is involved in both the positive and negative regulation of these processes. Cav1 exists in multiple cellular compartments depending on its role. Of particular interest is its contribution to the formation of plasma membrane invaginations called caveolae and its involvement in cytoskeletal interactions, endocytosis, and cholesterol trafficking. Cav1 participates in stem cell differentiation as well as proliferation and cell death pathways, which is implicated in tumor growth and metastasis. Additionally, Cav1 has tissue-specific functions that are adapted to the requirements of the cells within those tissues. Its role has been described in adipose, lung, pancreatic, and vascular tissue and in epithelial barrier maintenance. In both the intestinal and the blood brain barriers, Cav1 has significant interactions with junctional complexes that manage barrier integrity. Tight junctions have a close relationship with Cav1 and this relationship affects both their level of expression and their location within the cell. The ubiquitous nature of Cav1 both within the cell and within specific tissues is what makes the protein important for ongoing research as it can assist in further understanding pathophysiologic processes and can potentially be a target for therapies.

Citing Articles

The Non-Antibacterial Effects of Azithromycin and Other Macrolides on the Bronchial Epithelial Barrier and Cellular Differentiation.

Asbjarnarson A, Joelsson J, Gardarsson F, Sigurdsson S, Parnham M, Kricker J Int J Mol Sci. 2025; 26(5).

PMID: 40076911 PMC: 11900332. DOI: 10.3390/ijms26052287.


CAV1 promotes epithelial-to-mesenchymal transition (EMT) and chronic renal allograft interstitial fibrosis by activating the ferroptosis pathway.

Han Q, Ni B, Bao W, Zhang J, Zheng M, Miu J Front Immunol. 2025; 16:1523855.

PMID: 40013149 PMC: 11860899. DOI: 10.3389/fimmu.2025.1523855.


Genetic Manipulation of Caveolin-1 in a Transgenic Mouse Model of Aortic Root Aneurysm: Sex-Dependent Effects on Endothelial and Smooth Muscle Function.

Curry-Koski T, Gusek B, Potter R, Jones T, Dickman R, Johnson N Int J Mol Sci. 2024; 25(23).

PMID: 39684412 PMC: 11641669. DOI: 10.3390/ijms252312702.


Mechanisms of extracellular vesicle uptake and implications for the design of cancer therapeutics.

Jackson Cullison S, Flemming J, Karagoz K, Wermuth P, Mahoney M J Extracell Biol. 2024; 3(11):e70017.

PMID: 39483807 PMC: 11522837. DOI: 10.1002/jex2.70017.


Kaempferol promotes osteogenic differentiation in bone marrow mesenchymal stem cells by inhibiting CAV-1.

Li Y, Wang Y, Liu Q, Lv S, Wang Y, Zhang H J Orthop Surg Res. 2024; 19(1):678.

PMID: 39434162 PMC: 11495062. DOI: 10.1186/s13018-024-05174-0.


References
1.
Boscher C, Nabi I . Caveolin-1: role in cell signaling. Adv Exp Med Biol. 2012; 729:29-50. DOI: 10.1007/978-1-4614-1222-9_3. View

2.
Yamada E . The fine structure of the gall bladder epithelium of the mouse. J Biophys Biochem Cytol. 1955; 1(5):445-58. PMC: 2229656. DOI: 10.1083/jcb.1.5.445. View

3.
Park D, Lee H, Frank P, Razani B, Nguyen A, Parlow A . Caveolin-1-deficient mice show accelerated mammary gland development during pregnancy, premature lactation, and hyperactivation of the Jak-2/STAT5a signaling cascade. Mol Biol Cell. 2002; 13(10):3416-30. PMC: 129955. DOI: 10.1091/mbc.02-05-0071. View

4.
Xu Q, Shi W, Lv P, Meng W, Mao G, Gong C . Critical role of caveolin-1 in aflatoxin B1-induced hepatotoxicity via the regulation of oxidation and autophagy. Cell Death Dis. 2020; 11(1):6. PMC: 6952418. DOI: 10.1038/s41419-019-2197-6. View

5.
Yamamoto M, Toya Y, Schwencke C, Lisanti M, Myers Jr M, Ishikawa Y . Caveolin is an activator of insulin receptor signaling. J Biol Chem. 1998; 273(41):26962-8. DOI: 10.1074/jbc.273.41.26962. View