Role of the lncRNA MALAT1/miR-1 Pathway in Mouse Myocardial Ischemia-Reperfusion Injury

Introduction: The interplay between LncRNA MALAT1 and hsa-miR-1 plays a crucial role in Myocardial Ischemia-Reperfusion Injury (MIRI), offering insights into the molecular mechanisms underlying cardiovascular pathologies. This study sought to elucidate their regulatory relationship and functional impact on MIRI progression. Materials and Methods: Using an H9C2 cardiomyocyte cell line subjected to ischemia-reperfusion (I/R) modeling, we analyzed alterations in LncRNA MALAT1 and hsa-miR-1 expression and their downstream effects on apoptosis, reactive oxygen species (ROS) accumulation, and myocardial injury markers. Results: Our findings demonstrated that siRNA-mediated knockdown of MALAT1 or modulation of hsa-miR-1 (via mimics and inhibitors) effectively attenuated oxidative stress and reduced cardiomyocyte apoptosis. Furthermore, in vivo experiments using a murine MIRI model corroborated the regulatory roles of MALAT1 and hsa-miR-1, identifying them as potential therapeutic targets for mitigating reperfusion injury. Discussion: Our findings highlight the importance of the MALAT1/miR-1 axis in MIRI pathogenesis. The observed reduction in ROS and apoptosis upon modulation of these molecules suggests their involvement in key cellular stress responses. These results align with previous studies on lncRNA- miRNA interactions in cardiovascular diseases. Conclusion: These results not only highlight the significance of the MALAT1/miR-1 axis in MIRI but also propose novel molecular intervention strategies for the treatment of cardiovascular disease.