Predictors and prevention of diabetic cardiomyopathy

Chavali, Vishalakshi; Tyagi, Suresh C.; Mishra, Paras Kumar

doi:10.2147/dmso.s30968

Cited by 71 publications

(50 citation statements)

References 124 publications

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“…In our study, we observed that the polymorphism was nominally (P < 0.041) associated with higher risk of myocardial infarction in type 2 diabetes subjects. This would be in line with previous studies that have reported higher apoptosis in type 2 diabetic subjects [33,34,55], greater association between increased heart rate and cardiovascular morbid-mortality in type-2 diabetes subjects [29,30,56] and with studies showing that apoptosis in cardiomyocytes is a very important risk factor in triggering myocardial infarction [57,58]. However, in our study this association did not remain statistically significant after correction for multiple comparisons.…”

Section: Discussionsupporting

confidence: 92%

Novel association of the obesity risk-allele near Fas Apoptotic Inhibitory Molecule 2 (FAIM2) gene with heart rate and study of its effects on myocardial infarction in diabetic participants of the PREDIMED trial

Corella

Sorlí

González

et al. 2014

Cardiovasc Diabetol

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BackgroundThe Fas apoptotic pathway has been implicated in type 2 diabetes and cardiovascular disease. Although a polymorphism (rs7138803; G > A) near the Fas apoptotic inhibitory molecule 2 (FAIM2) locus has been related to obesity, its association with other cardiovascular risk factors and disease remains uncertain.MethodsWe analyzed the association between the FAIM2-rs7138803 polymorphism and obesity, blood pressure and heart rate in 7,161 participants (48.3% with type 2 diabetes) in the PREDIMED study at baseline. We also explored gene-diet interactions with adherence to the Mediterranean diet (MedDiet) and examined the effects of the polymorphism on cardiovascular disease incidence per diabetes status after a median 4.8-year dietary intervention (MedDiet versus control group) follow-up.ResultsWe replicated the association between the FAIM2-rs7138803 polymorphism and greater obesity risk (OR: 1.08; 95% CI: 1.01-1.16; P = 0.011; per-A allele). Moreover, we detected novel associations of this polymorphism with higher diastolic blood pressure (DBP) and heart rate at baseline (B = 1.07; 95% CI: 0.97-1.28 bmp in AA vs G-carriers for the whole population), that remained statistically significant even after adjustment for body mass index (P = 0.012) and correction for multiple comparisons. This association was greater and statistically significant in type-2 diabetic subjects (B = 1.44: 95% CI: 0.23-2.56 bmp; P = 0.010 for AA versus G-carriers). Likewise, these findings were also observed longitudinally over 5-year follow-up. Nevertheless, we found no statistically significant gene-diet interactions with MedDiet for this trait. On analyzing myocardial infarction risk, we detected a nominally significant (P = 0.041) association in type-2 diabetic subjects (HR: 1.86; 95% CI:1.03-3.37 for AA versus G-carriers), although this association did not remain statistically significant following correction for multiple comparisons.ConclusionsWe confirmed the FAIM2-rs7138803 relationship with obesity and identified novel and consistent associations with heart rate in particular in type 2 diabetic subjects. Furthermore, our results suggest a possible association of this polymorphism with higher myocardial infarction risk in type-2 diabetic subjects, although this result needs to be replicated as it could represent a false positive.

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Section: Discussionsupporting

confidence: 92%

Novel association of the obesity risk-allele near Fas Apoptotic Inhibitory Molecule 2 (FAIM2) gene with heart rate and study of its effects on myocardial infarction in diabetic participants of the PREDIMED trial

Corella

Sorlí

González

et al. 2014

Cardiovasc Diabetol

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“…The different roles of miR-133a in β-AR activation in diabetic and pressure-overload hearts suggest that miR-133a may normalize the contractility of diabetic hearts by targeting other upstream signaling molecules that activate β-AR in diabetic hearts. Another reason could be that the metabolic conditions in the diabetic heart differ from those in other failing hearts (9). Further, we overexpressed miR-133a in rats by delivering miR-133a mimic, whereas miR-133aTg mice were used in the pressure-overload model (27).…”

Section: Discussionmentioning

confidence: 99%

“…Diabetes mellitus (DM) is a complex disease caused due to insufficient insulin secretion from pancreatic β-cells (type 1 DM) and/or insulin resistance (type 2 DM) that results in an increased blood glucose level leading to morbidity and death (9). The number of patients with DM is increasing at an alarming rate in the world (10,11); however, the causes for the increased prevalence of DM and DM-mediated cardiomyopathy are poorly understood.…”

Section: Introductionmentioning

confidence: 99%

Lack of miR-133a Decreases Contractility of Diabetic Hearts: A Role for Novel Cross Talk Between Tyrosine Aminotransferase and Tyrosine Hydroxylase

et al. 2016

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MicroRNAs (miRNAs) have a fundamental role in diabetic heart failure. The cardioprotective miRNA-133a (miR-133a) is downregulated, and contractility is decreased in diabetic hearts. Norepinephrine (NE) is a key catecholamine that stimulates contractility by activating β-adrenergic receptors (β-AR). NE is synthesized from tyrosine by the rate-limiting enzyme, tyrosine hydroxylase (TH), and tyrosine is catabolized by tyrosine aminotransferase (TAT). However, the cross talk/link between TAT and TH in the heart is unclear. To determine whether miR-133a plays a role in the cross talk between TH and TAT and regulates contractility by influencing NE biosynthesis and/or β-AR levels in diabetic hearts, Sprague-Dawley rats and miR-133a transgenic (miR-133aTg) mice were injected with streptozotocin to induce diabetes. The diabetic rats were then treated with miR-133a mimic or scrambled miRNA. Our results revealed that miR-133a mimic treatment improved the contractility of the diabetic rat’s heart concomitant with upregulation of TH, cardiac NE, β-AR, and downregulation of TAT and plasma levels of NE. In miR-133aTg mice, cardiac-specific miR-133a overexpression prevented upregulation of TAT and suppression of TH in the heart after streptozotocin was administered. Moreover, miR-133a overexpression in CATH.a neuronal cells suppressed TAT with concomitant upregulation of TH, whereas knockdown and overexpression of TAT demonstrated that TAT inhibited TH. Luciferase reporter assay confirmed that miR-133a targets TAT. In conclusion, miR-133a controls the contractility of diabetic hearts by targeting TAT, regulating NE biosynthesis, and consequently, β-AR and cardiac function.

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“…Different stages of remodeling have been proposed, such as the early, advanced, and late stages [72]. …”

Section: Functional and Structural Alterationsmentioning

confidence: 99%

Diabetic cardiomyopathy: where we are and where we are going

Lee

Kim

2017

Korean J Intern Med

122

161

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The global burden of diabetes mellitus and its related complications are currently increasing. Diabetes mellitus affects the heart through various mechanisms including microvascular impairment, metabolic disturbance, subcellular component abnormalities, cardiac autonomic dysfunction, and a maladaptive immune response. Eventually, diabetes mellitus can cause functional and structural changes in the myocardium without coronary artery disease, a disorder known as diabetic cardiomyopathy (DCM). There are many diagnostic tools and management options for DCM, although it is difficult to detect its development and effectively prevent its progression. In this review, we summarize the current research regarding the pathophysiology and pathogenesis of DCM. Moreover, we discuss emerging diagnostic evaluation methods and treatment strategies for DCM, which may help our understanding of its underlying mechanisms and facilitate the identification of possible new therapeutic targets.

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Predictors and prevention of diabetic cardiomyopathy

Cited by 71 publications

References 124 publications

Novel association of the obesity risk-allele near Fas Apoptotic Inhibitory Molecule 2 (FAIM2) gene with heart rate and study of its effects on myocardial infarction in diabetic participants of the PREDIMED trial

Novel association of the obesity risk-allele near Fas Apoptotic Inhibitory Molecule 2 (FAIM2) gene with heart rate and study of its effects on myocardial infarction in diabetic participants of the PREDIMED trial

Lack of miR-133a Decreases Contractility of Diabetic Hearts: A Role for Novel Cross Talk Between Tyrosine Aminotransferase and Tyrosine Hydroxylase

Diabetic cardiomyopathy: where we are and where we are going

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