The study of the mechanism of non-coding RNA regulation of programmed cell death in diabetic cardiomyopathy

被引：1
作者：
Zhang, Bingrui [1 ]
Wu, Hua [2 ]
Zhang, Jingwen [1 ]
Cong, Cong [1 ]
Zhang, Lin [3 ]
机构：
[1] Shandong Univ Tradit Chinese Med, Affiliated Hosp, Cardiovasc Dept Cardiovasc Dis Res, Jinan 250014, Shandong, Peoples R China
[2] Taian Special Care Hosp Clin Lab Med Lab Direct, Tai An 271000, Shandong, Peoples R China
[3] Taian Hosp Chinese Med, Cardiovasc Dept Cardiovasc Dis Res, 216,Yingxuan St, Tai An 271000, Shandong, Peoples R China
来源：
MOLECULAR AND CELLULAR BIOCHEMISTRY | 2024年 / 479卷 / 07期
关键词：
Non-coding RNA; Programmed cell death; Diabetic cardiomyopathy; Mechanisms of action; INFLAMMATORY CASPASES; AUTOPHAGY; FERROPTOSIS; PYROPTOSIS; APOPTOSIS; NECROPTOSIS; CARDIOMYOCYTES; ACTIVATION; PHOSPHORYLATION; OVEREXPRESSION;
D O I：
10.1007/s11010-023-04909-7
中图分类号：
Q2 [细胞生物学];
学科分类号：
071009 ; 090102 ;
摘要：
Diabetic cardiomyopathy (DCM) represents a distinct myocardial disorder elicited by diabetes mellitus, characterized by aberrations in myocardial function and structural integrity. This pathological condition predominantly manifests in individuals with diabetes who do not have concurrent coronary artery disease or hypertension. An escalating body of scientific evidence substantiates the pivotal role of programmed cell death (PCD)-encompassing apoptosis, autophagy, pyroptosis, ferroptosis, and necroptosis-in the pathogenic progression of DCM, thereby emerging as a prospective therapeutic target. Additionally, numerous non-coding RNAs (ncRNAs) have been empirically verified to modulate the biological processes underlying programmed cell death, consequently influencing the evolution of DCM. This review systematically encapsulates prevalent types of PCD manifest in DCM as well as nascent discoveries regarding the regulatory influence of ncRNAs on programmed cell death in the pathogenesis of DCM, with the aim of furnishing novel insights for the furtherance of research in PCD-associated disorders relevant to DCM.
引用
收藏
页码：1673 / 1696
页数：24
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