MYL4, also known as myosin light chain 4, is crucial for muscle-related functions. It is involved in atrial development, atrial cardiomyopathy, determining muscle-fiber size, and muscle development processes like myoblast proliferation, migration, differentiation, and fusion [1,4,5,6]. It may also play a role in autophagic flux regulation in atrial cardiomyocytes [5]. Genetic models such as pigs and mice are valuable for studying MYL4.

In pigs, the SV of MYL4 was identified, and its genotype distribution differed between Ningxiang pigs and Large White pigs. Functional studies showed that overexpression of MYL4 in myoblasts inhibited proliferation and promoted apoptosis and differentiation, while knockdown had the opposite effect [1]. In Duchenne muscular dystrophy mouse models, increased Myl4 expression was observed in areas of muscle regeneration [2]. In a study on microplastics-induced cardiotoxicity in mice and human-originated cardiac organoids, the expression of cardiac-specific marker MYL4 was elevated [3]. In a zebrafish Myl4 knockout model, molecular, cellular, and physiologic abnormalities were found, paralleling those in humans with MYL4 mutations related to atrial fibrillation [7].

In conclusion, MYL4 is essential for muscle development and function, influencing myoblast behaviors, muscle fiber size, and having implications in muscle regeneration, cardiotoxicity, and atrial fibrillation. The use of gene knockout models in zebrafish and studies in other species like pigs and mice have provided insights into its role in these biological processes and disease conditions.