Rbpms, short for RNA binding protein with multiple splicing, is an RNA-binding protein that plays essential roles in RNA splicing regulation. It is involved in various biological processes, with significant importance in cardiac and retinal development and function [2,4,6]. Rbpms-associated pathways include those related to cytoskeletal signaling, which influence cardiomyocyte development and function [3]. Genetic models, such as mouse lines, are valuable tools for studying Rbpms function.

In cardiac-specific knockout mouse models, loss of Rbpms led to severe cardiomyocyte contractile defects, resulting in dilated cardiomyopathy and early lethality in adult mice. This was due to Rbpms regulating mRNA alternative splicing of genes associated with sarcomere structure and function, like Ttn, Pdlim5, and Nexn [1]. Additionally, genetic deletion of Rbpms in mice caused perinatal lethality because of congenital cardiovascular defects, with premature onset of cardiomyocyte binucleation and cell cycle arrest during development [3]. In Rbpms and Rbpms2 double cardiomyocyte-specific knockout mice, they died before embryonic day 13.5 with sarcomere disarray, highlighting the cooperative role of these two in safeguarding cardiac splicing [5].

In conclusion, Rbpms is crucial for cardiomyocyte contraction, cardiac function, and cardiovascular development, as demonstrated by gene-knockout mouse models. These models have revealed its significance in cardiac-related diseases, such as cardiomyopathy and congenital heart disease, providing insights into the molecular mechanisms underlying these conditions [1,3,5].