Clinical Approach to Diabetic Cardiomyopathy: A Review of Human Studies

Tarquini, Roberto; Pala, Laura; Brancati, Simona; Vannini, Giulia; Cosmo, Salvatore De; Mazzoccoli, Gianluigi; Rotella, Carlo Maria

doi:10.2174/0929867324666170705111356

Cited by 21 publications

(14 citation statements)

References 101 publications

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“…Patients with DCM often do not have heart failure symptoms even when LVW increases in the early stage, but as the disease progresses, cardiac enlargement decreases diastolic left ventricular lling, thereby causing left ventricular diastolic dysfunction. DCM can be seen under cardiac MRI mainly manifested as left ventricular hypertrophy, interstitial and peripheral vascular brosis and microvascular abnormalities [11]. This study found that compared with healthy rats, DCM rats showed a signi cant increase in LVW and a signi cant increase in the ratio of LVW to body weight, which also proved that the increase of LVW in DCM rats was not related to obesity, which was consistent with previous studies [10].…”

Section: Discussionsupporting

confidence: 91%

Effect and Mechanism of Sacubitril/valsartan on Ventricular Remodeling in STZ induced Diabetic Cardiomyopathy Rats

Tang¹,

Z²,

Ai³

et al. 2020

Preprint

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Background: Diabetic cardiomyopathy (DCM) has a high incidence of heart failure and poor prognosis, so its prevention and treatment should be more active. In this study, we investigate the effect and mechanism of sacubitril/valsartan (Sac/Val) on ventricular remodeling in DCM rats, so as to provide a new idea for clinical prevention of DCM.Methods: Twenty 8-week-old male Wistar rats were randomly divided into four groups: normal rat group (NOR), DCM group, DCM+ Sac/Val group and DCM+ Perindopril (PER) group , with 5 rats in each group. The DCM rat model was established by intraperitoneal injection of 1% streptozotocin (STZ). NOR and DCM groups were gavaged with normal saline (1ml/100g/d) for 8 weeks, while Sac/Val and PER groups were gavaged with Sac/Val (60mg/kg/d) and PER (2mg/kg/d) for 8 weeks. HE and Masson staining were used to evaluate the pathological changes of myocardial tissue, the left ventricular/ body mass index was calculated to evaluate ventricular remodeling, the levels of IL-6 and TNF- α in myocardial tissue were detected by ELISA, and the protein expression of p-38 and phos-p38 was detected. Results: Compared with the NOR group, the arrangement of cardio myocytes in the DCM group was disordered and the content of collagen fibers increased. In the DCM group, the left ventricular/body mass index increased, the levels of IL-6 and TNF- α increased, and the phos-p38 protein expression increased (P＜0.01). Compared with DCM group, fewer collagen fibers were found and the degree of fibrosis was reduced in Sac/Val group and PER group. The levels of left ventricular/body mass index, IL-6, TNF- α and phos-p38 protein expression in the Sac/Val group were all lower than those in the DCM group, and the differences were statistically significant (P＜0.01).Conclusion: Sac/Val can improve ventricular remodeling in DCM, and its mechanism may be related to its anti-inflammatory effect and inhibition of p38 signaling pathway in myocardial tissue.

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Section: Discussionsupporting

confidence: 91%

Effect and Mechanism of Sacubitril/valsartan on Ventricular Remodeling in STZ induced Diabetic Cardiomyopathy Rats

Tang¹,

Z²,

Ai³

et al. 2020

Preprint

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“…The risk of heart disease increases 2–3 times in diabetic patients. Diabetic mellitus (DM) is a common degenerative chronic metabolic disease that causes considerable negative impacts on health and lifespan with diabetic cardiovascular complications (DCCs) as major causes of death in diabetic population 1 , 2 , 3 , 4 , 5 . Diabetic cardiomyopathy (DCM) is one of the DCCs which literally account for more than 80% of diabetic deaths.…”

Section: Introductionmentioning

confidence: 99%

Preliminary evidence for the presence of multiple forms of cell death in diabetes cardiomyopathy

Wei

Zhao

Liang

et al. 2022

Acta Pharmaceutica Sinica B

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Diabetic mellitus (DM) is a common degenerative chronic metabolic disease often accompanied by severe cardiovascular complications (DCCs) as major causes of death in diabetic patients with diabetic cardiomyopathy (DCM) as the most common DCC. The metabolic disturbance in DCM generates the conditions/substrates and inducers/triggers and activates the signaling molecules and death executioners leading to cardiomyocyte death which accelerates the development of DCM and the degeneration of DCM to heart failure. Various forms of programmed active cell death including apoptosis, pyroptosis, autophagic cell death, autosis, necroptosis, ferroptosis and entosis have been identified and characterized in many types of cardiac disease. Evidence has also been obtained for the presence of multiple forms of cell death in DCM. Most importantly, published animal experiments have demonstrated that suppression of cardiomyocyte death of any forms yields tremendous protective effects on DCM. Herein, we provide the most updated data on the subject of cell death in DCM, critical analysis of published results focusing on the pathophysiological roles of cell death, and pertinent perspectives of future studies.

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“…It is estimated that DCM occurs in approximately 12% of diabetic patients (17). Clinical data suggests that DCM is closely associated with Clinical studies indicate that DCM increases the risk of overt heart failure and induces worse prognosis in diabetic patients (18).…”

Section: Discussionmentioning

confidence: 99%

METTL14 Suppresses Pyroptosis and Diabetic Cardiomyopathy by Down-Regulating TINCR lncRNA

Meng

Lin

Huang

et al. 2021

Preprint

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Background: N6-methyladenosine (m6A) is one of the most important epigenetic regulation of RNAs, such as lncRNAs. However, the underlying regulatory mechanism of m6A in diabetic cardiomyopathy (DCM) is very limited. In this study, we sought to define the role of METTL14-mediated m6A modification in pyroptosis and DCM progression.Methods: DCM rat model was established and qRT-PCR, western blot and immunohistochemistry (IHC) were used to detect the expression of METTL14 and TINCR. Gain-and-loss functional experiments were performed to define the role of METTL14-TINCR-NLRP3 axis in pyroptosis and DCM. RNA pulldown and RNA immunoprecipitation (RIP) assays were carried out to verify the underlying interaction.Results: In vivo and in vitro studies showed that pyroptosis was tightly involved in DCM progression. METTL14 was downregulated in cardiomyocytes and hear tissues of DCM rat tissues. Functionally, METTL14 suppressed pyroptosis and DCM via downregulating lncRNA TINCR, which further decreased the expression of key pyroptosis-related protein, NLRP3. Mechanistically, METTL14 increased m6A methylation level of TINCR gene, resulting in its downregulation. Moreover, the m6A reader protein YTHDF2 was essential for m6A methylation and mediated the degradation of TINCR. Finally, TINCR positively regulated NLRP3 through increasing its mRNA stability.Conclusions: Our work revealed the novel role of METTL14-mediated m6A methylation and lncRNA regulation in pyroptosis and DCM, which could help extend our understanding the epigenetic regulation of pyroptosis in DCM progression.

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Clinical Approach to Diabetic Cardiomyopathy: A Review of Human Studies

Abstract: The management of DC involves improvement in lifestyle, control of glucose and lipid abnormalities, together with treatment of hypertension and CAD, if present.

Cited by 21 publications

References 101 publications

Effect and Mechanism of Sacubitril/valsartan on Ventricular Remodeling in STZ induced Diabetic Cardiomyopathy Rats

Effect and Mechanism of Sacubitril/valsartan on Ventricular Remodeling in STZ induced Diabetic Cardiomyopathy Rats

Preliminary evidence for the presence of multiple forms of cell death in diabetes cardiomyopathy

METTL14 Suppresses Pyroptosis and Diabetic Cardiomyopathy by Down-Regulating TINCR lncRNA

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