Pparg, or peroxisome proliferator-activated receptor gamma, is a receptor that controls cellular metabolism and regulates the function of immune cells and stromal cells. It is involved in multiple anti-inflammatory and neuroprotective mechanisms in the CNS, and also plays a role in lipid and glucose metabolism [1,2].

In rheumatoid arthritis (RA), PPARG promotes autophagy to accelerate reactive oxygen species (ROS) clearance, inhibiting ROS-mediated macrophage polarization and NLRP3 inflammasome activation, which may distinguish RA patients from healthy controls and be a novel target for alleviating RA [1].

In major depression, the PPARg system increases BDNF levels, promotes neuroplasticity and neurogenesis, and may have antidepressant effects [2].

In adrenal Cushing's syndrome, PPARG and related genes are downregulated, and its activator rosiglitazone reduces cell viability and steroid production [3].

The Pro12Ala (rs1801282) genetic variant in PPARG is associated with a decreased risk of T2DM, and patients with the Ala12 variant respond better to thiazolidinediones treatment [4,5].

In bladder cancer, Pparg signaling controls cancer subtype and immune exclusion [6].

In psoriasis vulgaris, enhanced PPARG gene expression is a protective factor [7].

In hypopharyngeal squamous cell carcinoma, PPARG may promote chemosensitivity [8].

In summary, Pparg is crucial in various biological processes and disease conditions. Studies on Pparg-related genetic models have provided insights into its functions in diseases such as RA, major depression, adrenal Cushing's syndrome, T2DM, bladder cancer, psoriasis vulgaris, and hypopharyngeal squamous cell carcinoma, highlighting its potential as a therapeutic target.