Observational analysis reports that NFATc3 enhances angiogenesis in endothelial cells after myocardial infarction, indicating its therapeutic potential.
Key Points
NFATc3 promotes angiogenesis in endothelial cells, thereby mitigating cardiac injury after myocardial infarction.
Deletion of NFATc3 in endothelial cells impacts mitochondrial function and reduces angiogenesis, worsening heart damage.
NFATc3 upregulates lncRNA MALAT1, which is crucial for enhancing mitochondrial function in endothelial cells.
Targeting NFATc3 in endothelial cells offers a novel therapeutic strategy for myocardial infarction treatment.