Effects of non-coding RNAs and RNA-binding proteins on mitochondrial dysfunction in diabetic cardiomyopathy

被引:3
|
作者
Potel, Koray N. [1 ]
Cornelius, Victoria A. [1 ]
Yacoub, Andrew [1 ]
Chokr, Ali [2 ]
Donaghy, Clare L. [1 ]
Kelaini, Sophia [1 ]
Eleftheriadou, Magdalini [1 ]
Margariti, Andriana [1 ]
机构
[1] Queens Univ Belfast, Wellcome Wolfson Inst Expt Med, Sch Med Dent & Biomed Sci, Belfast, North Ireland
[2] Univ Picardie Jules Verne, Fac Med, Amiens, France
来源
关键词
diabetes mellitus; diabetic cardiomyopathy; mitochondrial dysfunction; noncoding RNAs; RNA-binding proteins; stem cell modelling; OXIDATIVE STRESS; UP-REGULATION; CARDIAC-HYPERTROPHY; DOWN-REGULATION; CONTRACTILE DYSFUNCTION; DIASTOLIC DYSFUNCTION; SUBSTRATE METABOLISM; INSULIN-RESISTANCE; CELL-PROLIFERATION; CALCIUM-TRANSPORT;
D O I
10.3389/fcvm.2023.1165302
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Vascular complications are the main cause of diabetes mellitus-associated morbidity and mortality. Oxidative stress and metabolic dysfunction underly injury to the vascular endothelium and myocardium, resulting in diabetic angiopathy and cardiomyopathy. Mitochondrial dysfunction has been shown to play an important role in cardiomyopathic disruptions of key cellular functions, including energy metabolism and oxidative balance. Both non-coding RNAs and RNA-binding proteins are implicated in diabetic cardiomyopathy, however, their impact on mitochondrial dysfunction in the context of this disease is largely unknown. Elucidating the effects of non-coding RNAs and RNA-binding proteins on mitochondrial pathways in diabetic cardiomyopathy would allow further insights into the pathophysiological mechanisms underlying diabetic vascular complications and could facilitate the development of new therapeutic strategies. Stem cell-based models can facilitate the study of non-coding RNAs and RNA-binding proteins and their unique characteristics make them a promising tool to improve our understanding of mitochondrial dysfunction and vascular complications in diabetes.
引用
收藏
页数:17
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