Shroom3, encoding an actin-associated protein, is the sole member of the SHROOM protein group regulating actin dynamics via apical constriction and apicobasal cell elongation. It is involved in multiple biological processes, and its function is crucial in development and disease-related pathways [1].

In kidney-related studies, Shroom3-deficient mouse models have provided significant insights. Shroom3Gt/+ mice with 22-minute ischemic injury showed increased mortality, worsened kidney function, and disrupted epithelial redifferentiation, Rho-kinase/myosin signaling, and apical F-actin organization, indicating its importance in epithelial repair and redifferentiation after AKI and its link to CKD [2]. Shroom3 knockdown in mice led to albuminuria and podocyte foot process effacement, and in vitro, it caused defective lamellipodia formation in podocytes, disrupting the slit diaphragm, suggesting its role in maintaining podocyte structure and kidney function [4].

In optic cup development, Shroom3-deficient mouse embryos had coloboma phenotypes due to increased apical cell areas, disrupted optic fissure alignment, and failure to re-establish apical-basal polarity, highlighting its role in epithelial fusion events [3].

In cardiac development, Shroom3gt/gt mice exhibited a spectrum of congenital heart defects, demonstrating that SHROOM3 functions as an actomyosin cytoskeleton effector downstream of the planar cell polarity signaling pathway [5].

In conclusion, Shroom3 is essential for various biological processes such as epithelial morphogenesis, kidney function maintenance, optic cup development, and cardiac development. The study of Shroom3 KO/CKO mouse models has significantly contributed to understanding its roles in kidney diseases, ocular development, and congenital heart diseases, providing valuable insights into the underlying molecular mechanisms and potential therapeutic targets.