Mef2c, a transcription factor of the MADS-BOX family, is involved in numerous biological processes. It plays a crucial role in embryonic brain development, neuronal formation and differentiation, axon and dendrite growth and pruning. It is also associated with pathways related to macrophage polarization, lipid metabolism, and ferroptosis, and is of great biological importance in various physiological and pathological conditions. Genetic models, such as KO/CKO mouse models, have been valuable for studying Mef2c's functions.

Myeloid-specific Mef2c-knockout mice showed reduced IL-12 production and impaired Th1 responses, leading to susceptibility to Listeria monocytogenes infection and protection against DSS-induced IBD, revealing its role in macrophage polarization and Th1 responses [1]. In meningioma, MEF2C silencing enhanced Erastin-induced ferroptotic cell death, and in vivo, MEF2C knockdown augmented Erastin's anti-meningioma effect [2]. MEF2C-haploinsufficient patients and mice had defects in NK cell development and effector function, with increased susceptibility to viral infection, and MEF2C regulated lipid content through SREBP pathways in NK cells [3]. In mice, anesthesia and surgery decreased MEF2C levels in the hippocampus, and MEF2C overexpression alleviated postoperative memory decline by repressing ferroptosis [4]. Conditional deletions of Mef2cfl/fl with either Col1-Cre or Dmp1-Cre in mice produced generalized high bone mass, suggesting its role in bone mass regulation [5].

In conclusion, Mef2c is essential for multiple biological processes. Model-based research, especially KO/CKO mouse models, has revealed its significance in diseases such as inflammatory and autoimmune diseases, meningioma, viral infections, postoperative cognitive dysfunction, and bone-related disorders. Understanding Mef2c provides insights into disease mechanisms and potential therapeutic targets.