Sustained miRNA release regenerates the heart

Insight into Heart-Tailored Architectures of Hydrogel to Restore Cardiac Functions after Myocardial Infarction

“…However, the scar tissue in the heart cannot compensate for the lack of the contractile property and would cause mechanical dysfunction, circulatory deficiency and a lack of pump function, culminating in HF. 25 After being injected into the myocardium, the therapeutic agents are highly possible to be washed out from the target site via venous drainage or squeeze under continuous cardiac pulsation. Although repeated administrations are tried to sustain effective drug levels in vivo, the overflowed drugs may cause side effects to neighbor tissues.…”

“…139,140 Constitutive expression of the miRNA cluster in the mice heart can cause cardiomyopathy, due to highly proliferative and persistently dedifferentiated immature cardiomyocytes. 25 Regulating miR-34a or its target genes (Sirt1, Cyclin D1 and Bcl2) can exert effects in function of ADAR2 in the antiapoptosis and pro-proliferation, wherein ADAR2 is an enzyme with ability to edit adenosine to inosine nucleotides in double-stranded RNA. 141 MiR-222 acts as a necessary factor for exercise-induced cardiomyocyte proliferation and growth in the adult mammalian heart, whose overexpression was found to prevent adverse remodeling after MI.…”

“…With the ability to simultaneously promote endogenous molecule secretion and regulate multiple gene levels, noncoding RNA (ncRNA) shows potential in stimulating cardiac regeneration in the ischemic heart, including microRNA (miRNA), circular RNA and long noncoding RNA (lncRNA) . A cluster of miRNAs (miR-302/367) can induce cardiomyocyte proliferation by inhibiting the Hippo signaling pathway. , Constitutive expression of the miRNA cluster in the mice heart can cause cardiomyopathy, due to highly proliferative and persistently dedifferentiated immature cardiomyocytes . Regulating miR-34a or its target genes (Sirt1, Cyclin D1 and Bcl2) can exert effects in function of ADAR2 in the antiapoptosis and pro-proliferation, wherein ADAR2 is an enzyme with ability to edit adenosine to inosine nucleotides in double-stranded RNA .…”

“…Compromised by the minimal regeneration ability of the heart, damaged myocardium post-MI cannot regenerate cardiomyocytes, thereby forming a scar tissue without contractile. However, the scar tissue in the heart cannot compensate for the lack of the contractile property and would cause mechanical dysfunction, circulatory deficiency and a lack of pump function, culminating in HF . After being injected into the myocardium, the therapeutic agents are highly possible to be washed out from the target site via venous drainage or squeeze under continuous cardiac pulsation.…”