Molecular Basis of Cardiomyopathies in Type 2 Diabetes

被引:1
|
作者
Giardinelli, Silvia [1 ]
Meliota, Giovanni [2 ]
Mentino, Donatella [3 ]
D'Amato, Gabriele [4 ]
Faienza, Maria Felicia [3 ]
机构
[1] Univ Ferrara, Dept Med Sci, Pediat, I-44121 Ferrara, Italy
[2] Giovanni XXIII Pediat Hosp, Dept Pediat Cardiol, I-70126 Bari, Italy
[3] Univ Bari Aldo Moro, Dept Precis & Regenerat Med & Ionian Area, Pediat Unit, I-70124 Bari, Italy
[4] Venere Hosp, Neonatal Intens Care Unit, I-70012 Bari, Italy
关键词
type; 2; diabetes; diabetic cardiomyopathy; heart failure; cardiac remodeling; epigenetics; molecular mechanisms; Glucagon-like Peptide-1 (GLP-1) receptor agonists; gliflozins; therapeutic approaches; SARCOPLASMIC-RETICULUM CA2+-ATPASE; RENIN-ANGIOTENSIN SYSTEM; GLYCATION END-PRODUCTS; OXIDATIVE STRESS; CARDIAC-HYPERTROPHY; DNA METHYLATION; GENE-EXPRESSION; HIGH GLUCOSE; PROMOTER METHYLATION; INSULIN-RESISTANCE;
D O I
10.3390/ijms25158280
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Diabetic cardiomyopathy (DbCM) is a common complication in individuals with type 2 diabetes mellitus (T2DM), and its exact pathogenesis is still debated. It was hypothesized that chronic hyperglycemia and insulin resistance activate critical cellular pathways that are responsible for numerous functional and anatomical perturbations in the heart. Interstitial inflammation, oxidative stress, myocardial apoptosis, mitochondria dysfunction, defective cardiac metabolism, cardiac remodeling, hypertrophy and fibrosis with consequent impaired contractility are the most common mechanisms implicated. Epigenetic changes also have an emerging role in the regulation of these crucial pathways. The aim of this review was to highlight the increasing knowledge on the molecular mechanisms of DbCM and the new therapies targeting specific pathways.
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页数:21
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