A study in humans demonstrated that the mir-208a is a cardiac-specific miRNA deregulated in patients with acute coronary syndrome and acute myocardial infarction [Tong et al. DOI:10.3390/ijms19051467]. Research in a rat model of post-infarction heart failure identified rno-miR-208a-3p as significantly downregulated in heart failure tissue, with its expression increasing early post-myocardial infarction but decreasing in later stages, and therapeutic silencing of miR-208a is noted to prevent pathological cardiac remodeling [Liu et al. DOI:10.1371/journal.pone.0160920]. A study in mice demonstrated that the mir-208a showed a sustained increase in expression upon myocardial infarction specifically in cardiomyocytes compared to other cell types [Kumar Maji et al. DOI:10.1038/s41597-025-05061-1].