TABLE 1.

Therapies for treating MIRI by targeting non-coding RNAs to regulate autophagy.

Treatment	Non-coding RNAs served as druggable targets	Mechanism	References
Puerarin	LncRNA ANRIL	Puerarin improved cardiomyocyte activity, and alleviated the MIRI by upregulation of ANRIL, which reduced LDH and MDA levels, inhibited the H/R induced autophagy and apoptosis of cardiomyocytes	Han et al. (2021)
Morphine	UCA1/miR-128	Morphine Postconditioning educed the size of myocardial infarction by inhibiting autophagy and apoptosis via regulation of UCA1/miR-128/HSP7 axis	Chen et al. (2018)
Citrate	miR-142-3p	Citrate pretreatment inhibited cell apoptosis and autophagy induced by H/R injury, decreased LDH and MDA levels, and alleviated H/R injury by miR-142-3p/Rac1 aix	Xiang et al. (2020)
Exosome	miR-30a	The miR-30a inhibitors carried by exosomes could reduce the contents of AST, CPK and MDA in serum, increase the activity of SOD, inhibit the expression of ULK1 and Beclin-1, reduce autophagy, and inhibit the apoptosis of myocardial cells in MIRI rats	Xu et al. (2019)
Bone Marrow Mesenchymal Stem Cell Derived Exosomal (BMMSCs)	miR-29c	Exosomes derived from BMMSCs contained high concentrations of miR-29C, which attenuated MIRI by inhibiting excessive autophagy via PTEN/Akt/mTOR signaling pathway	Li et al. (2020a)
Epigallocatechin gallate (EGCG)	miR-384-5p	EGCG preconditioning increased cell viability and reduced the size of myocardial infarction through adjusting miR-384-5p targets Beclin-1 to attenuate the expression of the I/R-induced autophagy flux via PI3K/Akt pathway	Zhang et al. (2019a)
salvianolic acid B (Sal B)	miR-30a	Sal B regulated Beclin-1 through miR-30/PI3K/Akt pathway, which inhibited I/R-induced autophagy, improved cell viability, reduced LDH leakage and alleviated MIRI.	Li et al. (2016)
Mesenchymal stem cells (MSCs)	let-7b	MSCs modified with let-7b could improve the survival rate of transplanted cells, reduce infarct size and promote the repair of myocardial injury by reducing the expression of autophagy-related genes BECN1, ATG5, ATG7 and ATG12	Ham et al. (2015)
Rosuvastatin (RS)	miR-17-3p	RS could promote autophagy, reduce LDH leakage and improve cell viability by inhibiting miR-17-3p. It could also reduce apoptosis by cleaved caspase-3/Cyto C signaling pathway	Wang X. et al. (2019)
Sevoflurane	miR-206	Sevoflurane post-conditioning could inhibit autophagy, apoptosis, and myocardial fibrosis, promote free radical clearance, promote free radical clearance, and improve MIRI by inhibiting miR-206 to activate AMPK/Nampt signaling pathway	Li et al. (2020b)
Sevoflurane	miR-208a	Sevoflurane post-conditioning could enhance SOD activity, inhibit the expression of MDA and facilitate the activation of the PI3K/AKT pathway via inhibition of miR-208a, thereby alleviating MIRI.	Shi et al. (2020)
Propofol	miR-20b-5p	Propofol preconditioning reduced apoptosis, and alleviated H/R injury via upregulation of mib-20b-5p, which targeted ULK1 to inhibit autophagy	Zhen et al. (2020)
Hypoxia postconditioning (HPostC)	miR-30a	HPostC promoted the expression of miR-30a through DNMT3b, thereby inhibiting BECN1-mediated autophagy and alleviating H/R injury. It is speculated that Ischemic postconditioning (IPostC) can also reduce I/R injury of elderly cardiac myocytes by targeting miR-30a	Wang et al. (2020)
Osthole	miR-30a	Osthole could promote autophagy by down-regulating miR-30a to reduce collagen content in ischemic reperfusion myocardium, inhibit myocardial apoptosis combined with myocardial injury, and alleviate MIRI.	Liu et al. (2019)
Salidroside	circ-0000064	Salidroside inhibited autophagy and apoptosis of cells by upregulation of CIRC-0000064, which improved myocardial function, decreased SOD, MDA, CK-MB and LDH levels, inhibited oxidative stress, reduced myocardial infarction size, thus alleviating MIRI	Jin et al. (2021)