Diabetic cardiomyopathy

Lorenzo-Almorós, Ana; Cepeda-Rodrigo, José María; Lorenzo, Óscar

doi:10.1016/j.rceng.2019.10.012

Cited by 26 publications

(33 citation statements)

References 168 publications

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“…DCM is a special cardiac complication characterized by chronic cardiomyopathy caused by diabetes 10 . The pathological process includes oxidative stress, energy metabolism, inflammatory reaction and increased myocardial cell apoptosis in cardiac myocytes 10 , 63 (Table 2 ).…”

Section: Molecular Mechanisms Of Mitochondrial Dysfunction In Dcmmentioning

confidence: 99%

Mitochondrial quality control in diabetic cardiomyopathy: from molecular mechanisms to therapeutic strategies

Cai¹,

Wu²,

He³

et al. 2022

Int. J. Biol. Sci.

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In diabetic cardiomyopathy (DCM), a major diabetic complication, the myocardium is structurally and functionally altered without evidence of coronary artery disease, hypertension or valvular disease. Although numerous anti-diabetic drugs have been applied clinically, specific medicines to prevent DCM progression are unavailable, so the prognosis of DCM remains poor. Mitochondrial ATP production maintains the energetic requirements of cardiomyocytes, whereas mitochondrial dysfunction can induce or aggravate DCM by promoting oxidative stress, dysregulated calcium homeostasis, metabolic reprogramming, abnormal intracellular signaling and mitochondrial apoptosis in cardiomyocytes. In response to mitochondrial dysfunction, the mitochondrial quality control (MQC) system (including mitochondrial fission, fusion, and mitophagy) is activated to repair damaged mitochondria. Physiological mitochondrial fission fragments the network to isolate damaged mitochondria. Mitophagy then allows dysfunctional mitochondria to be engulfed by autophagosomes and degraded in lysosomes. However, abnormal MQC results in excessive mitochondrial fission, impaired mitochondrial fusion and delayed mitophagy, causing fragmented mitochondria to accumulate in cardiomyocytes. In this review, we summarize the molecular mechanisms of MQC and discuss how pathological MQC contributes to DCM development. We then present promising therapeutic approaches to improve MQC and prevent DCM progression.

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Section: Molecular Mechanisms Of Mitochondrial Dysfunction In Dcmmentioning

confidence: 99%

Mitochondrial quality control in diabetic cardiomyopathy: from molecular mechanisms to therapeutic strategies

Cai¹,

Wu²,

He³

et al. 2022

Int. J. Biol. Sci.

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“…Diabetic cardiomyopathy is a common complication of diabetes. Due to metabolic disorders and microvascular lesions, diabetic cardiomyopathy leads to extensive focal myocardial necrosis and subclinical cardiac dysfunction, which eventually develops into heart failure, arrhythmia, cardiac shock and even sudden death in severe cases (1)(2)(3) Rutin is a flavonoid compound extracted from plants, and has been reported to exert antioxidant, anti-inflammatory, anti-allergic and anti-viral effects (4,5). Rutin is thought to act on multiple tissues and organs in the body.…”

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Rutin alleviates cardiomyocyte injury induced by high glucose through inhibiting apoptosis and endoplasmic reticulum stress

Wang

et al. 2021

Exp Ther Med

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Diabetic cardiomyopathy is a common complication of diabetes, in which endoplasmic reticulum stress (ERS) serves an important role. Rutin can treat the myocardial dysfunction of diabetic rats. However, to the best of our knowledge, studies on the effects of Rutin on myocardial injury caused by diabetes from the perspective of ERS have not previously been reported. In the present study, the role of rutin in the regulation of ERS in myocardial injury was assessed. Different high glucose concentrations were used to treat H9C2 myoblast cells to establish a myocardial damage model. A cell counting kit-8 assay was used to determine cell viability. A lactate dehydrogenase kit was used to detect cytotoxicity. Apoptosis levels were determined using a TUNEL assay. Western blotting was used to determine the expression levels of apoptosis-related proteins and ERS-related proteins, including heat shock protein A family member 5, inositol-requiring enzyme-1α, X-box binding protein 1, activating transcription factor 6, C/EBP-homologous protein (CHOP), cleaved caspase-12 and caspase-12. The anti-apoptotic and anti-ERS effects of Rutin on H9C2 cardiac cells induced by high glucose were examined after the administration of the ERS activator thapsigargin (TG). The results indicated that rutin could dose-dependently inhibit the level of apoptosis and ERS induced by high glucose in H9C2 cells. After administration of the ERS activator TG, it was demonstrated that TG could reverse the anti-apoptotic and anti-ERS effects of rutin on H9C2 cells stimulated with high glucose. Collectively, the present results suggested that rutin may alleviate cardiomyocyte model cell injury induced by high glucose through the inhibition of apoptosis and ERS.

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“…Similar to the current study, Muhammad and Hashmi [ 36 ] reported an elevation in serum creatinine (>1.5) in DCM patients compared with diabetic patients without cardiomyopathy. However, further cohort studies are still needed among patients with DCM to assess the diagnostic and prognostic utility of serum biomarkers and their normal ranges to establish therapeutic strategies in order to prevent disease progression [ 37 ].…”

Section: Discussionmentioning

confidence: 99%

Role of Some Serum Biomarkers in the Early Detection of Diabetic Cardiomyopathy

Abdelrahman

Salama

et al. 2021

Future Sci. OA

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Aim: To assess the role of serum biomarkers in early prediction of diabetic cardiomyopathy. Materials and methods: The participants were three groups of Type 2 diabetes mellitus (DM) patients having diastolic dysfunction (DM-DD), systolic dysfunction (DM-SD) and normal echocardiography (DM-N) with two control groups: non-DM diastolic dysfunction patients (DD) and healthy controls. AGEs, TNF-α, IL-6, IGFBP-7, creatinine and insulin were assessed. Results: TNF-α, AGEs, creatinine and insulin panel had area under the curve (AUC) of 0.913 in distinguishing DM-DD from DM-N (78.7% sensitivity and 100% specificity). IL-6 and AGEs panel had AUC 0.795 for differentiating DM-SD from DM-DD (90.6% sensitivity). IL-6, TNF-α and AGEs panel had AUC 0.924 for differentiating diabetic cardiomyopathy from DM-N (85% sensitivity and specificity). Conclusion: A panel of AGEs, IL-6, TNF-α, insulin and creatinine might be used for early detection of DM-DD among T2DM patients.

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Diabetic cardiomyopathy

Cited by 26 publications

References 168 publications

Mitochondrial quality control in diabetic cardiomyopathy: from molecular mechanisms to therapeutic strategies

Mitochondrial quality control in diabetic cardiomyopathy: from molecular mechanisms to therapeutic strategies

Rutin alleviates cardiomyocyte injury induced by high glucose through inhibiting apoptosis and endoplasmic reticulum stress

Role of Some Serum Biomarkers in the Early Detection of Diabetic Cardiomyopathy

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