Mitochondrial NAD<sup>+</sup>/NADH Redox State and Diabetic Cardiomyopathy

Berthiaume, Jessica M.; Kurdys, Jacob; Muntean, Daniela-Lucia; Roșca, Mariana G.

doi:10.1089/ars.2017.7415

Cited by 133 publications

(105 citation statements)

References 205 publications

(275 reference statements)

Supporting

Mentioning

103

Contrasting

Order By: Relevance

“…The NAD + /NADH ratio indicates the activity of various metabolic pathway enzymes, such as those involved in mitochondrial oxidation as the predominant energy source. Notably, a previous study demonstrated that a decreased NAD + /NADH ratio was associated with diabetic cardiomyopathy [23]. Our results revealed that mice transplanted with PAI-1KO scWAT had a significantly increased NAD + / NADH ratio in cardiac tissues compared with that in the WT and sham groups, suggesting that targeting PAI-1 is necessary for preventing the metabolic complications caused by obesity and T2DM.…”

Section: Discussionsupporting

confidence: 57%

Transplantation of adipose tissue lacking PAI-1 improves glucose tolerance and attenuates cardiac metabolic abnormalities in high-fat diet-induced obesity

Liu

Fan

et al. 2020

Adipocyte

View full text Add to dashboard Cite

show abstract

Section: Discussionsupporting

confidence: 57%

Transplantation of adipose tissue lacking PAI-1 improves glucose tolerance and attenuates cardiac metabolic abnormalities in high-fat diet-induced obesity

Liu

Fan

et al. 2020

Adipocyte

View full text Add to dashboard Cite

show abstract

“…The NAD + /NADH ratio is a sensitive marker of the cellular redox state [93]. In fact, ROS production by activity of complex I depends on the matrix redox potential, and as a consequence, the increase in NAD + /NADH triggers PGC-1α deacetylation through SIRT1 activation [94].…”

Section: Tissue-specificmentioning

confidence: 99%

PGC-1α, Inflammation, and Oxidative Stress: An Integrative View in Metabolism

Rius‐Pérez

Torres-Cuevas

Millán

et al. 2020

Oxidative Medicine and Cellular Longevity

432

292

View full text Add to dashboard Cite

Peroxisome proliferator-activated receptor-γ coactivator (PGC)-1α is a transcriptional coactivator described as a master regulator of mitochondrial biogenesis and function, including oxidative phosphorylation and reactive oxygen species detoxification. PGC-1α is highly expressed in tissues with high energy demands, and it is clearly associated with the pathogenesis of metabolic syndrome and its principal complications including obesity, type 2 diabetes mellitus, cardiovascular disease, and hepatic steatosis. We herein review the molecular pathways regulated by PGC-1α, which connect oxidative stress and mitochondrial metabolism with inflammatory response and metabolic syndrome. PGC-1α regulates the expression of mitochondrial antioxidant genes, including manganese superoxide dismutase, catalase, peroxiredoxin 3 and 5, uncoupling protein 2, thioredoxin 2, and thioredoxin reductase and thus prevents oxidative injury and mitochondrial dysfunction. Dysregulation of PGC-1α alters redox homeostasis in cells and exacerbates inflammatory response, which is commonly accompanied by metabolic disturbances. During inflammation, low levels of PGC-1α downregulate mitochondrial antioxidant gene expression, induce oxidative stress, and promote nuclear factor kappa B activation. In metabolic syndrome, which is characterized by a chronic low grade of inflammation, PGC-1α dysregulation modifies the metabolic properties of tissues by altering mitochondrial function and promoting reactive oxygen species accumulation. In conclusion, PGC-1α acts as an essential node connecting metabolic regulation, redox control, and inflammatory pathways, and it is an interesting therapeutic target that may have significant benefits for a number of metabolic diseases.

show abstract

“…Besides, exercise improves glucose metabolism in the diabetic myocardium and pancreas. Long-term regular exercise has been shown to decrease nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, increase nitric oxide synthase and nitric oxide production, and enhance anti-oxidative activity in the endothelial cells [73]. The nuclear factor erythroid 2-related factor 2 (Nrf2) is crucial for defending cardiomyocytes against intracellular oxidative stress, and as a regulator of antioxidant response elements [74][75][76][77][78].…”

Section: Oxidative Stress In Cardiomyocytesmentioning

confidence: 99%

Exercise as A Potential Therapeutic Target for Diabetic Cardiomyopathy: Insight into the Underlying Mechanisms

Seo

Jang

et al. 2019

IJMS

View full text Add to dashboard Cite

Diabetes mellitus is associated with cardiovascular, ophthalmic, and renal comorbidities. Among these, diabetic cardiomyopathy (DCM) causes the most severe symptoms and is considered to be a major health problem worldwide. Exercise is widely known as an effective strategy for the prevention and treatment of many chronic diseases. Importantly, the onset of complications arising due to diabetes can be delayed or even prevented by exercise. Regular exercise is reported to have positive effects on diabetes mellitus and the development of DCM. The protective effects of exercise include prevention of cardiac apoptosis, fibrosis, oxidative stress, and microvascular diseases, as well as improvement in cardiac mitochondrial function and calcium regulation. This review summarizes the recent scientific findings to describe the potential mechanisms by which exercise may prevent DCM and heart failure.

show abstract

Mitochondrial NAD⁺/NADH Redox State and Diabetic Cardiomyopathy

Cited by 133 publications

References 205 publications

Transplantation of adipose tissue lacking PAI-1 improves glucose tolerance and attenuates cardiac metabolic abnormalities in high-fat diet-induced obesity

Transplantation of adipose tissue lacking PAI-1 improves glucose tolerance and attenuates cardiac metabolic abnormalities in high-fat diet-induced obesity

PGC-1α, Inflammation, and Oxidative Stress: An Integrative View in Metabolism

Exercise as A Potential Therapeutic Target for Diabetic Cardiomyopathy: Insight into the Underlying Mechanisms

Contact Info

Product

Resources

About

Mitochondrial NAD+/NADH Redox State and Diabetic Cardiomyopathy

Cited by 133 publications

References 205 publications

Transplantation of adipose tissue lacking PAI-1 improves glucose tolerance and attenuates cardiac metabolic abnormalities in high-fat diet-induced obesity

Transplantation of adipose tissue lacking PAI-1 improves glucose tolerance and attenuates cardiac metabolic abnormalities in high-fat diet-induced obesity

PGC-1α, Inflammation, and Oxidative Stress: An Integrative View in Metabolism

Exercise as A Potential Therapeutic Target for Diabetic Cardiomyopathy: Insight into the Underlying Mechanisms

Contact Info

Product

Resources

About

Mitochondrial NAD⁺/NADH Redox State and Diabetic Cardiomyopathy