Cavin2, also known as serum deprivation protein response (SDPR), is a protein-coding gene related to caveolae. Caveolae are important for various cellular functions like endocytosis, cell membrane assembly, and signal transduction. Cavin2 forms complexes with other caveola-related proteins and is involved in multiple biological pathways, playing a significant role in normal physiological and pathological processes [5,6]. Genetic models, such as gene knockout mouse models, are valuable for studying Cavin2's functions.

Systemic Cavin2 knockout in mice induced mild cardiomyocyte (CM) hypertrophy under stress-free conditions, and after swim training, CM hypertrophy was more facilitated with enhanced phosphoinositide 3-kinase (PI3K)-Akt activity [6]. In cardiac-specific Cavin2 conditional knockout (Cavin-2 cKO) mice, CM hypertrophy and apoptosis were suppressed in an Angiotensin II-induced pathological cardiac hypertrophy model [6].

In lung cancer, Cavin2 is frequently silenced by CpG methylation. Overexpression of Cavin2 inhibits lung cancer cell migration, invasion, and proliferation by inducing G2/M cell cycle arrest, and it sensitizes lung cancer cells to paclitaxel and 5-fluorouracil [1]. In lung adenocarcinoma, Cavin2 functions as a tumor suppressor, and its overexpression inhibits cell proliferation and migration due to cell apoptosis induction and cell cycle arrest at S phase [2].

In ventilator-induced lung injury (VILI) in rats, Cavin2 can bind to ERK1/2 and inhibit the activation of the MAPK/ERK1/2 signaling pathway, reducing inflammatory response and autophagy, thus attenuating lung injury [3].

In intervertebral disc degeneration, Cavin2 plays a role in the uptake process of extracellular vesicles (EVs), and Cavin-2-modified engineering EVs can effectively retard the progression of intervertebral disc degeneration [4].

In breast cancer, Cavin2 acts as a suppressor, inhibiting breast cancer progression by blocking the transforming growth factor (TGF-β) signaling pathway [5].

In conclusion, Cavin2 plays diverse biological functions. Through gene knockout and conditional knockout mouse models, its role in various disease areas has been revealed, including cardiac hypertrophy, lung cancer, ventilator-induced lung injury, intervertebral disc degeneration, and breast cancer. These findings contribute to a better understanding of the underlying mechanisms of these diseases and may provide potential therapeutic targets.