Mir208a, a cardiac-specific microRNA, plays a key role in modulating gene expression in the heart. It is involved in various cardiac-related processes such as heart development, function, and pathogenesis. It participates in pathways related to cardiac hypertrophy, remodeling, electrophysiology, and the regulation of myofiber genes. Additionally, it may assist in governing systemic energy homeostasis by modulating the "endocrine" function of cardiac muscle [1].

Genetic deletion of miR-208a in rodents attenuated stress-induced cardiac hypertrophy and remodeling, indicating its key role in these processes [1]. Also, mechanical stretch-induced miR-208a expression in cultured rat cardiomyocytes and myoblasts is mediated by TGF-β1, and miR-208a is involved in stretch-induced cardiac hypertrophy and may lead to cardiac fibrosis [2,3]. Blocking the function of miR-208a with anti-miR-208a increased ZEB2 expression in the heart and effectively protected from the development of pathological cardiac hypertrophy, suggesting miR-208a's role in regulating genes related to calcium-handling and contractility [4].

In conclusion, Mir208a is crucial for cardiac function, being deeply involved in processes like cardiac hypertrophy, remodeling, and regulation of calcium-handling genes. Studies using gene knockout (KO) models in rodents have been instrumental in revealing its role in these processes, providing insights into the molecular mechanisms underlying heart diseases.