Sorbs2, also known as Sorbin and SH3 Domain Containing 2, is ubiquitously expressed in various tissues including the cardiovascular system. It serves as a cytoskeletal adaptor and an RNA-binding protein. Sorbs2 is involved in regulating the expression and function of proteins like the BK channel in vascular smooth muscle cells, and may be associated with pathways related to inflammation, lipid metabolism, and synaptic transmission [1]. Its function is crucial for maintaining normal physiological processes in the body, and genetic models such as KO mouse models are valuable for studying its role.

In KO mouse models, Sorbs2 knockout in cardiomyocytes leads to dilated cardiomyopathy, with defective microtubule polymerization and compensatory upregulation of structural cytoskeletal and adapter proteins responsible for contractile dysfunction [3]. Sorbs2 knockout mice at 4 months also display a decrease in BK channel expression and function in coronary arteries, mimicking the vasculopathy seen in diabetic mice [1]. In human embryonic stem cell differentiation models, knockdown of SORBS2 disrupts sarcomeric integrity of cardiomyocytes and reduces cardiomyocyte number [2].

In conclusion, Sorbs2 is essential for maintaining the structural integrity of cardiomyocytes and regulating BK channel function in vascular smooth muscle cells. Studies using KO mouse models have revealed its significant role in cardiovascular diseases, including dilated cardiomyopathy and diabetic vasculopathy, providing insights into the mechanisms of these diseases and potential therapeutic targets.