MYL3, also known as myosin light chain 3, is a gene encoding a sarcomeric protein. Sarcomeric proteins are essential for muscle contraction, and thus, MYL3 is crucial for normal muscle function. Mutations in this gene have been associated with hypertrophic cardiomyopathy and other related cardiac diseases, highlighting its significance in cardiac health [2,3,4,5,6,7,8,9].

In chondrocytes, MYL3 has been shown to play a protective role against senescence. Conditional deletion of Myl3 in chondrocytes of male mice significantly promoted osteoarthritis (OA) progression, while intra-articular injection of adeno-associated virus overexpressing MYL3 delayed OA progression. MYL3 deficiency enhanced clathrin-mediated endocytosis by promoting the interaction between myosin VI and clathrin, leading to the internalization of Notch and activation of Notch signaling in chondrocytes. Blocking this signaling pathway prevented MYL3 loss-induced chondrocyte senescence and alleviated OA progression [1].

In conclusion, MYL3 is essential for maintaining normal muscle function, especially in the context of cardiac health and chondrocyte senescence. Studies using gene knockout and overexpression models in mice have revealed its role in inhibiting chondrocyte senescence and thus potentially preventing OA development. In the context of cardiomyopathies, understanding MYL3 mutations can contribute to better diagnosis and management of hypertrophic cardiomyopathy.