Mrtfa, also known as Megakaryoblastic Leukemia 1 (MKL1), is a coactivator of serum response factor (SRF). It couples transcriptional regulation to actin cytoskeleton dynamics, and the MRTFA-SRF complex's transcriptional targets include cytoskeletal protein-encoding genes and immediate early genes. Mrtfa is involved in many critical cellular functions such as cell growth, apoptosis, and differentiation of various cell types including muscle and hematopoietic cells [1].

Knockout of either SRF or Mrtfa in primary hematopoietic cells decreases megakaryocyte (Mk) maturation, leading to thrombocytopenia. In HEL cells, Mrtfa overexpression enhances megakaryopoiesis by increasing SRF's genomic association and activity, and upregulating genes promoting megakaryopoiesis [2]. In cardiomyocytes, Cypher/ZASP deficiency leads to F-actin destabilization, increased G-actin levels, impaired Mrtfa nuclear localization, and abnormal cardiomyocyte maturation. Re-expression of SRF can rectify these defects [3]. In human coronary artery smooth muscle cells, Mrtfa promotes lipid accumulation, and its inhibition reduces lipid accumulation, suggesting it could be a therapeutic target for vascular lipid-related diseases [4].

In conclusion, Mrtfa is crucial in multiple biological processes. Studies using gene knockout models in hematopoietic cells, cardiomyocytes, and smooth muscle cells have revealed its roles in megakaryocyte maturation, cardiomyocyte maturation, and lipid homeostasis in the vasculature. These findings contribute to understanding the pathogenesis of related diseases and offer potential therapeutic directions.