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, regulating important biological processes. It is involved in pathways related to ion channel regulation, cell-matrix interactions, and inflammation, which are crucial for normal physiological functions [1,2]. Genetic models like knockout mice are valuable for studying its functions.

In gene knockout studies, Sorbs2-knockout mice at 4 months old showed decreased BK channel expression and function in coronary arteries, along with impaired Ca2 +-sensitivity and vasodilation, mimicking diabetic vascular phenotypes [2]. Cardiomyocyte-specific Sorbs2 knockout (Sorbs2-cKO) mice developed progressive systolic dysfunction, enlarged cardiac chambers, and died of congestive heart failure around 1 year old. Early intracellular structural remodeling due to defective microtubule polymerization was found to be responsible for contractile dysfunction [3].

In conclusion, Sorbs2 is essential for maintaining the structural integrity of cardiomyocytes and regulating ion channel functions in blood vessels. The Sorbs2 KO/CKO mouse models have significantly contributed to understanding its role in cardiovascular diseases, providing insights into potential disease mechanisms and possible therapeutic targets in this area.