Parim B, Sathibabu V V, Saravanan G. Diabetic cardiomyopathy: molecular mechanisms, detrimental effects of conventional treatment, and beneficial effects of natural therapy[J]. Heart Fail Rev,2019, 24(2):279-299.
[5]
Prabhu M, Yaxuan L, David K, et al. Angiogenic mechanisms of Human CD34+ stem cell exosomes in the repair of ischemic hindlimb[J]. Circ Res, 2017, 120(9): 1466-1476.
[6]
Xie F, Zhou X, Fang M, et al. Extracellular vesicles in cancer immune microenvironment and cancer immunotherapy[J]. Adv Sci (Weinh), 2019, 6(24):.
[7]
Hathaway Q A, Pinti M V, Durr A J, et al. Regulating microRNA expression: at the heart of diabetes mellitus and the mitochondrion[J]. Am J Physiol Heart Circ Physiol, 2018, 314(2): H293-H310.
[8]
Bellin G, Gardin C, Ferroni L, et al. Exosome in cardiovascular diseases: a complex world full of hope[J]. Cells, 2019, 8(2):166.
Jia G, Hill M A, Sowers J R. Diabetic cardiomyopathy: an update of mechanisms contributing to this clinical entity[J]. Circ Res, 2018, 122(4):624-638.
[11]
Adlakha Y K, Seth P. The expanding horizon of miRNAs in cellular reprogramming[J]. Prog Neurobiol, 2017, 148:21-39.
[12]
Xue R, Tan W, Wu Y, et al. Role of exosomal miRNAs in heart failure[J]. Front Cardiovasc Med, 2020, 7:592412.
[13]
Jia G, Whaley C A,Sowers J R. Diabetic cardiomyopathy: a hyperglycaemia- and insulin-resistance-induced heart disease[J]. Diabetologia, 2018, 61(1): 21-28.
[14]
Nirmala K, Abdoh T,Zhou J F, et al. Pharmacological strategies to lower crosstalk between nicotinamide adenine dinucleotide phosphate (NADPH) oxidase and mitochondria[J]. Biomed Pharmacother, 2019, 111: 1478-1498.
[15]
Samarjit D, Mark K, Brittany D E, et al. Divergent effects of mir-181 family members on myocardial function through protective cytosolic and detrimental mitochondrial miRNA targets[J]. J Am Heart Assoc, 2017, 6(3): e004694.
[16]
Azzouzi H, Leptidis S, Dirkx E, et al. The hypoxia-inducible microRNA cluster miR-199a~214 targets myocardial PPARδ and impairs mitochondrial fatty acid oxidation[J].Cell Metab, 2013, 18(3):341-354.
[17]
Singh R M, Waqar T, Howarth F C, et al. Hyperglycemia-induced cardiac contractile dysfunction in the diabetic heart[J]. Heart Fail Rev, 2018, 23(1): 37-54.
[18]
Chen C, Yang S L, Li H P, et al. Mir30c is involved in diabetic cardiomyopathy through regulation of cardiac autophagy via BECN1[J]. Mol Ther Nucleic Acids, 2017, 7(C): 127-139.
[19]
Zhang W, Xu W T,Feng Y, et al. Non-coding RNA involvement in the pathogenesis of diabetic cardiomyopathy[J]. J Cell Mol Med, 2019, 23(9): 5859-5867.
[20]
Feng B, Chen S L, George B, et al. Mir133a regulates cardiomyocyte hypertrophy in diabetes[J]. Diabetes Metab Res Rev, 2010, 26(1): 40-49.
[21]
Ma Q, Ma Y, Wang X N, et al. Circulating mir-1 as a potential predictor of left ventricular remodeling following acute st-segment myocardial infarction using cardiac magnetic resonance[J]. Quant Imaging Med Surg, 2020, 10(7): 1490-1503.
[22]
Yu F, Chapman S, Pham D L, et al. Decreased mir-150 in obesity-associated type 2 diabetic mice increases intraocular inflammation and exacerbates retinal dysfunction[J]. BMJ Open Diabetes Res Care, 2020, 8(1):e001446.
[23]
Gabriela P D, Takano A P, Maria L M. MiRNA-208a and miRNA-208b are triggered in thyroid hormone-induced cardiac hypertrophy-role of type 1 nngiotensin II receptor (AT1R) on miRNA-208a/α-MHC modulation[J]. Mol Cell Endocrinol, 2013, 374(1-2): 117-124.
[24]
Raut S K, Singh G B, Rastogi B, et al. MiR-30c and mir-181a synergistically modulate p53-p21 pathway in diabetes induced cardiac hypertrophy[J]. Mol Cell Biochem, 2016, 417(1-2):191-203.
[25]
Wei H, Bu R,Yang Q H, et al. Exendin-4 protects against hyperglycemia-induced cardiomyocyte pyroptosis via the AMPK-TXNIP pathway[J]. J Diabetes Res, 2019, 2019:8905917.
[26]
Lee S, Suh G Y,Ryter S W, et al. Regulation and function of the nucleotide binding domain leucine-rich repeat-containing receptor, pyrin domain-containing-3 inflammasome in lung disease[J]. Am J Respir Cell Mol Biol, 2016, 54(2): 151-160.
[27]
Zhu Y, Qian X,Li J, et al. Astragaloside-Ⅳ protects H9C2(2-1) cardiomyocytes from high glucose-induced injury via miR-34a-mediated autophagy pathway[J]. Artificial Cells, 2019, 47(1): 4172-4181.
[28]
Yu X Y, Song Y H, Geng Y J, et al. Glucose induces apoptosis of cardiomyocytes via microRNA-1 and IGF-1[J]. BBRC, 2008, 376(3):548-552.
[29]
Delfan M, Delphan M,Kordi M R, et al. High intensity interval training improves diabetic cardiomyopathy via miR-1 dependent suppression of cardiomyocyte apoptosis in diabetic rats[J]. J Diabetes Metab Disord, 2020, 19(1): 145-152.
[30]
Nilanjan G, Rajesh K. Molecular mechanism of diabetic cardiomyopathy and modulation of microRNA function by synthetic oligonucleotides[J]. Cardiovasc Diabetol, 2018, 17(1): 43.
[31]
Feng B, Cao Y,Chen S L, et al. MiR-200b mediates endothelial-to-mesenchymal transition in diabetic cardiomyopathy[J]. Diabetes, 2016, 65(3): 768-779.
[32]
Li X, Meng C,Han F, et al. Vildagliptin attenuates myocardial dysfunction and restores autophagy via miR-21/SPRY1/ERK in diabetic mice heart[J]. Front Pharmacol, 2021,12:634365.
[33]
Eva V R, Lillian B S,Jeffrey E T, et al. Dysregulation of microRNAs after myocardial infarction reveals a role of miR-29 incardiac fibrosis[J]. Proc Natl Acad Sci.U S A, 2008, 105(35): 13027-13032.
[34]
Jane C, Hana F, Bing Y X, et al. PARP mediates structural alterations in diabetic cardiomyopathy[J]. J Mol Cell Cardiol, 2008, 45(3): 385-393.
[35]
Lee W S, Kim J. Application of animal models in diabetic cardiomyopathy[J]. Diabetes Metab J,2021,45(2):129-145.
2021, Vol. 32 
