Zhang, J.; Yu, X.; Zheng, S.; Qiao, G.; Zhang, C.; Tang, S.; Gao, X.; Wang, Y.; Yu, Y.; Cheng, J.; Lei, M.; Li, P.; Yang, Y.; Zhang, C.; Yuan, Q.

DICAR-JP, a functional domainof DICAR, is a potent cardiocyte protective RNA via regulating protein degradation or translation in diabetic cardiomyopathy (DCM). Using AGEs to found the cell impairment model in vivo. Using SPR to investigate the binding interaction between DICAR-JP and the binding protein nascent polypeptide-associated complex (NAC). DICAR-JP is demonstrated the functional domain that interacts with NAC to regulate OGDHL nascent peptide expression. DICAR-JP facilitated the translocation of OGDHL nascent peptides from the cytoplasm to the mitochondria using in vitro translation approach, leading us to hypothesize that DICAR-JP plays a key role in regulating ribosomal migration from the endoplasmic reticulum to the mitochondria, which we refer to this process as the \'Ribosome Migration\'. DICAR-JP reversed the metabolic reprogramming observed in diabetic cardiomyocytes induced by AGEs. We optimized DICAR-JP sequence. DICAR-JP and DICAR-JP45 both exhibited significant cardioprotective effects against DCM, comparable to those observed with Dapagliflozin. Together, our results founded a new theory of mitochondrium enengry regulated protein originally from nuclear, the \'Ribosome Migration\'. And a new nucleic acid-based therapeutic candidate for treating DCM.