# Revolutionizing Autoimmune Research: The Role of Caveolin‐1

**Authors:** Yanan Gao, Liangyu Mi, Yingren Deng, Zhaojun Jia, Miaomiao Zhao, Yuting Hu, Yuli Ji, Xiaoyao He, Ke Xu

PMC · DOI: 10.1002/iid3.70230 · Immunity, Inflammation and Disease · 2025-08-08

## TL;DR

This paper explores how Caveolin-1 influences autoimmune diseases and highlights its potential as a diagnostic marker and treatment target.

## Contribution

The paper systematically reviews the role of Caveolin-1 in various autoimmune diseases, emphasizing its potential as a diagnostic and therapeutic target.

## Key findings

- Caveolin-1 regulates immune and inflammatory signaling pathways in autoimmune diseases.
- Caveolin-1 is increasingly recognized as a biomarker in several autoimmune conditions.
- Future research on Caveolin-1 may lead to new diagnostic and therapeutic strategies for autoimmune diseases.

## Abstract

Caveolins (Cav) include Cav‐1, Cav‐2, and Cav‐3, with Cav‐1 being the most studied due to its prominent role as a major component of plasma membrane caveolae. Cav‐1 is involved in a wide range of cellular functions and plays a key role in regulating signaling pathways related to immune responses and inflammation. Recently, research on Cav‐1 in autoimmune diseases (AIDs) has garnered significant interest.

This paper provides an overview of the research on Cav‐1's involvement in AIDs, including rheumatoid arthritis, systemic lupus erythematosus, Sjögren syndrome, anti‐neutrophil cytoplasmic antibody‐associated vasculitis, systemic sclerosis, connective tissue disease‐associated interstitial lung disease, autoimmune disorders of the nervous system, autoimmune uveitis, autoimmune thyroid disease, and autoimmune myocarditis.

Cav‐1 plays a critical role in various AIDs, acting as a key protein in inflammatory and immune cells. It regulates multiple signaling processes by controlling the translocation of signaling molecules and modulating various pathways. Cav‐1 is increasingly recognized as a biomarker in certain AIDs and may become pivotal in treating these diseases in the future.

Cav‐1 is a crucial player in the pathogenesis of many AIDs and has the potential to serve as both a diagnostic marker and a therapeutic target for these diseases. As research into Cav‐1 deepens, it may offer new insights into the diagnosis, treatment, and drug sensitivity of AIDs, emerging as a promising target for future therapeutic strategies.

## Linked entities

- **Genes:** CAV1 (caveolin 1) [NCBI Gene 857], CAV2 (caveolin 2) [NCBI Gene 858], CAV3 (caveolin 3) [NCBI Gene 859]
- **Proteins:** CAV1 (caveolin 1)
- **Diseases:** rheumatoid arthritis (MONDO:0008383), systemic lupus erythematosus (MONDO:0007915), Sjögren syndrome (MONDO:0010030), anti-neutrophil cytoplasmic antibody-associated vasculitis (MONDO:0015492), systemic sclerosis (MONDO:0005100), autoimmune disorders of the nervous system (MONDO:0002977), autoimmune uveitis (MONDO:0031012), autoimmune thyroid disease (MONDO:0005623), autoimmune myocarditis (MONDO:0022519)

## Full-text entities

- **Genes:** CAV3 (caveolin 3) [NCBI Gene 859] {aka LGMD1C, LQT9, MPDT, RMD2, VIP-21, VIP21}, CAV2 (caveolin 2) [NCBI Gene 858] {aka CAV}, CAV1 (caveolin 1) [NCBI Gene 857] {aka BSCL3, CGL3, LCCNS, MSTP085, PPH3, VIP21}
- **Diseases:** autoimmune myocarditis (MESH:D009205), systemic lupus erythematosus (MESH:D008180), inflammation (MESH:D007249), anti-neutrophil cytoplasmic antibody-associated vasculitis (MESH:D056648), Sjogren syndrome (MESH:D012859), systemic sclerosis (MESH:D012595), autoimmune uveitis (MESH:D014605), interstitial lung disease (MESH:D017563), autoimmune disorders of the nervous system (MESH:D020274), connective tissue disease (MESH:D003240), autoimmune thyroid disease (MESH:D013967), AIDs (MESH:D001327), rheumatoid arthritis (MESH:D001172)

## Full text

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## Figures

2 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12332503/full.md

## References

130 references — full list in the complete paper: https://tomesphere.com/paper/PMC12332503/full.md

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Source: https://tomesphere.com/paper/PMC12332503