TP53 and congestive heart failure: Wang et al. [107] showed that a miR-351 agomir effectively inhibited mixed lineage kinase 3 (MLK3) protein and mRNA expression to regulate JNK/p53 signaling pathway-mediated oxidative stress, which significantly increased the left ventricular ejection fraction (LVEF) and left ventricular fractional shortening (LVFS), decreased the left ventricular end-diastolic diameter (LVEDD), the left ventricular end-systolic diameter (LVESD), LV mass and collagen deposition, improved cardiac function, and inhibited cardiac hypertrophy and fibrosis in the advanced stage of congestive heart failure (CHF).