Cardiac fibrosis and dysfunction in experimental diabetic cardiomyopathy are ameliorated by alpha-lipoic acid

Li, Chunjun; Lin, Liang‐Chuan; Li, Hui; Yu, Di

doi:10.1186/1475-2840-11-73

Cited by 154 publications

(109 citation statements)

References 39 publications

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“…Studies with natural antioxidants such as vitamin E, vitamin C, and a-lipoic acid have yielded promising results in animal models of diabetes, particularly when STZ is used to induce hyperglycemia (7,57). However, when investigated in humans, these antioxidants either alone or in combination have not shown consistent beneficial effects on serum metabolic parameters or the incidence of cardiovascular disease (65,108).…”

Section: Antioxidant Therapiesmentioning

confidence: 99%

The Mitochondria in Diabetic Heart Failure: From Pathogenesis to Therapeutic Promise

Schilling

2015

Antioxidants & Redox Signaling

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Significance: Diabetes is an important risk factor for the development of heart failure (HF). Given the increasing prevalence of diabetes in the population, strategies are needed to reduce the burden of HF in these patients. Recent Advances: Diabetes is associated with several pathologic findings in the heart including dysregulated metabolism, lipid accumulation, oxidative stress, and inflammation. Emerging evidence suggests that mitochondrial dysfunction may be a central mediator of these pathologic responses. The development of therapeutic approaches targeting mitochondrial biology holds promise for the management of HF in diabetic patients. Critical Issues: Despite significant data implicating mitochondrial pathology in diabetic cardiomyopathy, the optimal pharmacologic approach to improve mitochondrial function remains undefined. Future Directions: Detailed mechanistic studies coupled with more robust clinical phenotyping will be necessary to develop novel approaches to improve cardiac function in diabetes. Moreover, understanding the interplay between diabetes and other cardiac stressors (hypertension, ischemia, and valvular disease) will be of the utmost importance for clinical translation of scientific discoveries made in this field. Antioxid. Redox Signal. 22, 1515Signal. 22, -1526

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Section: Antioxidant Therapiesmentioning

confidence: 99%

The Mitochondria in Diabetic Heart Failure: From Pathogenesis to Therapeutic Promise

Schilling

2015

Antioxidants & Redox Signaling

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“…Autophagy is involved in the intracellular degradation of type I collagen for the prevention of excess ECM deposition (3,72,82). There is also evidence that impaired autophagy promotes differentiation of fibroblasts to myofibroblasts, the profibrotic phenotype of fibroblasts (2,96). Although studies have reported increased activation of cardiac fibroblasts and fibrosis in diabetic hearts, no studies have examined whether autophagy plays a role in this response.…”

Section: Autophagy In Cell Types Beyond the Cardiomyocytementioning

confidence: 99%

Unbreak My Heart: Targeting Mitochondrial Autophagy in Diabetic Cardiomyopathy

Kubli

Gustafsson

2015

Antioxidants & Redox Signaling

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Significance: Diabetes is strongly associated with increased incidence of heart disease and mortality due to development of diabetic cardiomyopathy. Even in the absence of cardiovascular disease, cardiomyopathy frequently arises in diabetic patients. Current treatment options for cardiomyopathy in diabetic patients are the same as for nondiabetic patients and do not address the causes underlying the loss of contractility. Recent Advances: Although there are numerous distinctions between Type 1 and Type 2 diabetes, recent evidence suggests that the two disease states converge on mitochondria as an epicenter for cardiomyocyte damage. Critical Issues: Accumulation of dysfunctional mitochondria contributes to cardiac tissue injury in both acute and chronic conditions. Removal of damaged mitochondria by macroautophagy, termed ''mitophagy,'' is critical for maintaining cardiomyocyte health and contractility both under normal conditions and during stress. However, very little is known about the involvement of mitophagy in the pathogenesis of diabetic cardiomyopathy. A growing interest in this topic has given rise to a wave of publications that aim at deciphering the status of autophagy and mitophagy in Type 1 and Type 2 diabetes. Future Directions: This review summarizes these recent studies with the goal of drawing conclusions about the activation or suppression of autophagy and mitophagy in the diabetic heart. A better understanding of how autophagy and mitophagy are affected in the diabetic myocardium is still needed, as well as whether they can be targeted therapeutically. Antioxid. Redox Signal. 22, 1527Signal. 22, -1544

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“…Alpha lipoic acid (ALA), also named as thiotic acid, is a natural cofactor that is synthesized inside the plant and animal mitochondria (Thaakur and Himabindhu, 2009). ALA has recently used as a protective agent for many pathological alterations that are due to oxidative stress (Li et al, 2012 andWang et al, 2013). The antioxidant activity of ALA may discussed by its ability to scavenge free radicals in both lipophilic and hydrophilic environments, and to restore endogenous antioxidants, chelate transition metals, decrease lipid oxidation, prevent protein glycation and repair oxidatively damaged biomolecules (Palaniyappan and Alphonse, 2011).…”

Section: Introductionmentioning

confidence: 99%

Potential Ameliorative Effects of Alpha Lipoic Acid and Silymarin on Thioacetamide-Induced Hepatic Damage in Rats

Salama¹,

Oda²,

Khafaga³

et al. 2017

AJVS

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Key words:liver, thioacetamide, silymarin, alpha lipoic acid, rats.The present study was designed to study the ameliorative role of alpha lipoic acid (ALA) and silymarin (SIL) against thioacetamide (TAA)-induced hepatic damage. Sixty male albino rats were randomly separated into 6 groups (n=10); control group, TAA-treated group: received intraperitoneal injection of TAA 250 mg/kg bwt/day three times a week, ALAtreated group: received ALA 100 mg/kg bwt/day) orally three times a week, SIL-treated group: received SIL 100 mg/kg bwt/day orally three times a week, TAA+ALA-treated group, and TAA+SIL-treated group at the same previous doses and routes for ten weeks. Results showed that TAA induced a significant elevation in total and direct bilirubin, total cholesterol and triglycerides levels and serum liver enzymes after four and ten weeks of the treatments. While the serum levels of total proteins, albumin and high density lipoproteincholesterol revealed a significant decrease. TAA injection resulted in an increase in the hepatic lipid peroxidation and decreased levels of antioxidant biomarker. Histopathologically, TAA revealed marked degenerative, necrotic and fibrotic alterations in the liver, particularly during ten weeks post-treatment. ALA and SIL-treatment ameliorated TAA-induced oxidative damage, alterations in the liver function tests and liver histopathology. However, ALA demonstrated better hepatic protection against TAAinduced liver damage as compared to SIL. The study clearly concluded that ALA has more powerful antioxidant properties than SIL.

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Cardiac fibrosis and dysfunction in experimental diabetic cardiomyopathy are ameliorated by alpha-lipoic acid

Cited by 154 publications

References 39 publications

The Mitochondria in Diabetic Heart Failure: From Pathogenesis to Therapeutic Promise

The Mitochondria in Diabetic Heart Failure: From Pathogenesis to Therapeutic Promise

Unbreak My Heart: Targeting Mitochondrial Autophagy in Diabetic Cardiomyopathy

Potential Ameliorative Effects of Alpha Lipoic Acid and Silymarin on Thioacetamide-Induced Hepatic Damage in Rats

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