Myocardial infarction (MI) triggers complex pathological processes, including inflammation, hypoxia, and fibrotic remodeling. MicroRNAs (miRNAs) have emerged as promising biomarkers for cardiovascular injury; however, their expression dynamics along processes remain underexplored. We used an in vivo rat model of permanent coronary occlusion to study the molecular alterations associated with MI and its resolution in a temporal mode, including five experimental groups with five animals in each: sham, PO 24 h, PO 72 h, PO 7 d, PO 1 month. Histological analysis, serum biomarkers, and miRNA/gene expression profiles were analyzed in a time-dependent manner post-occlusion. Subsequent analysis revealed early depletion of selected circulating miRNAs (PO 24 h). Transient upregulation in cardiac tissue miRNAs, inflammatory and fibrotic gene expression (Fibronectin, Collagen, Vimentin, E-Cadherin) were observed at PO 72 h. These molecular alterations correlated with histological evidence of myocardial injury and repair. Taken together, our findings delineate the molecular timeline of MI progression and resolution and identify candidate miRNAs as sensitive and time-dependent indicators of myocardial stress, including miR-107, miR-122-5p and miR-221-3p. This integrative approach supports the use of miRNA signatures for noninvasive monitoring of cardiac injury and resolution and unveils potential therapeutic targets to reduce pathological remodeling.

We previously established that Multifrequency Electromagnetic Pulse (MEMP) treatment selectively eradicates tumorigenic cells in vitro. While this treatment proved safe in mice and prevented tumor formation by pre-treated cells, its efficacy against established tumors remained unknown. Here we evaluate the therapeutic effect of two different systemic MEMP treatment regimens (30 Hz, >2 T) on syngeneic MC38 colon adenocarcinoma es-tablished subcutaneously in C57BL/6 mice. The impact of MEMP on anti-tumor immune infiltration (CD4, CD8, CD68) responses, as well as oxidative stress (HO-1, MDA), and DNA damage (γH2AX), cell biology markers, were analyzed by immunohistochemistry. The MEMP regimes significantly reduced the growth of the xenografted tumors leading to an apparent regression in a small subset of animals, and extended survival without af-fecting animal welfare. Of note, mice that achieved complete tumor regression mounted a protective immune response, demonstrating robust resistance to a subsequent tumor re-challenge, indicative of immunological memory. Importantly, the quantitative penetra-tion of immune effectors CD68+ cells into tumors suggests the involvement of a strong, macrophage-mediated anti-tumor response, although the ultimate mechanisms driving the MEMP effects in vivo deserve further research. These findings place MEMP as a prom-ising anti-cancer treatment and a strong candidate procedure for combination with other systemic immunotherapies.