Serum Response Factor (SRF), a MADS-box transcription factor, is essential for various biological processes. It controls gene transcription, regulating cell proliferation, differentiation, migration, and cytoskeletal organization. SRF is involved in multiple signaling pathways, such as those related to VEGF and FGF during angiogenesis, and its activity is also associated with the pathogenesis of numerous diseases [3,4,6]. Genetic models, like KO/CKO mouse models, are valuable for studying SRF's functions.

In a mouse model of amyotrophic lateral sclerosis (ALS), ablation of SRF in motoneurons (MNs) of SOD1G93A mice led to earlier disease onset, accompanied by mild neuroinflammation and neuromuscular synapse degeneration. SRF-deficient MNs showed impaired induction of autophagy-encoding genes, suggesting its role in autophagy regulation [7]. In vascular smooth muscle cells (VSMCs), Senp1 deficiency increased SUMOylated SRF and the SRF-ELK complex, promoting vascular remodeling and neointimal formation. Targeting the SRF complex may be a potential therapy for cardiovascular diseases (CVD) [2,5]. In liver fibrosis, the SRF/MRTF-A complex is crucial, as MRTF-A translocates to the nucleus upon fibrotic pathway induction, forming an active complex that leads to the expression of fibrotic proteins. Silencing or inhibiting MRTF-A could be a therapeutic approach for liver cirrhosis [1].

In conclusion, SRF is a key transcription factor involved in a wide range of biological functions. Through model-based research, especially KO/CKO mouse models, its role in diseases like ALS, CVD, and liver cirrhosis has been revealed. Understanding SRF's functions provides potential therapeutic directions for these diseases.