PARP-1 inhibition alleviates diabetic cardiac complications in experimental animals

Zakaria, Esraa M.; El-Bassossy, Hany M.; El-Maraghy, Nabila N.; Aljawadi, Ahmed; Ali, Abdelmoneim A.

doi:10.1016/j.ejphar.2016.09.008

Cited by 32 publications

(15 citation statements)

References 47 publications

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“…TherapeuticinhibitionofotherPARPenzymes(specifically PARP1)hasalsobeenshowntoconfercardioprotectiveeffects, 32 as well as to reduce circulating TNF-α levels in vivo. 33 Although the inconsistency of the PARP14 finding across studies merits close attention in future investigations, our analysis contributes to growing evidence linking PARP enzymes with systemic inflammation and CHD. 31…”

Section: Discussionmentioning

confidence: 87%

Association of Methylation Signals With Incident Coronary Heart Disease in an Epigenome-Wide Assessment of Circulating Tumor Necrosis Factor α

et al. 2018

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Section: Discussionmentioning

confidence: 87%

Association of Methylation Signals With Incident Coronary Heart Disease in an Epigenome-Wide Assessment of Circulating Tumor Necrosis Factor α

et al. 2018

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“…The hindering mechanisms act through the poly-ADP-ribose polymerase (PARP) pathway, which alters GAPDH through polymers of ADP-ribose. Hyperglycemia provokes overproduction of ROS [ 99 ] and DNA single-strand cracks [ 100 ], both of which can stimulate PARP [ 101 ], thereby resulting in an alteration of GAPDH and a decrease of its activity [ 102 ] ( Figure 2 ).…”

Section: Diabetes and Oxidative Stressmentioning

confidence: 99%

Association of Glycemic Indices (Hyperglycemia, Glucose Variability, and Hypoglycemia) with Oxidative Stress and Diabetic Complications

Papachristoforou

Lambadiari

Maratou

et al. 2020

Journal of Diabetes Research

266

177

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Oxidative stress (OS) is defined as a disturbance in the prooxidant-antioxidant balance of the cell, in favor of the former, which results in the antioxidant capacity of the cell to be overpowered. Excess reactive oxygen species (ROS) production is very harmful to cell constituents, especially proteins, lipids, and DNA, thus causing damage to the cell. Oxidative stress has been associated with a variety of pathologic conditions, including diabetes mellitus (DM), cancer, atherosclerosis, neurodegenerative diseases, rheumatoid arthritis, ischemia/reperfusion injury, obstructive sleep apnea, and accelerated aging. Regarding DM specifically, previous experimental and clinical studies have pointed to the fact that oxidative stress probably plays a major role in the pathogenesis and development of diabetic complications. It is postulated that hyperglycemia induces free radicals and impairs endogenous antioxidant defense systems through several different mechanisms. In particular, hyperglycemia promotes the creation of advanced glycation end-products (AGEs), the activation of protein kinase C (PKC), and the hyperactivity of hexosamine and sorbitol pathways, leading to the development of insulin resistance, impaired insulin secretion, and endothelial dysfunction, by inducing excessive ROS production and OS. Furthermore, glucose variability has been associated with OS as well, and recent evidence suggests that also hypoglycemia may be playing an important role in favoring diabetic vascular complications through OS, inflammation, prothrombotic events, and endothelial dysfunction. The association of these diabetic parameters (i.e., hyperglycemia, glucose variability, and hypoglycemia) with oxidative stress will be reviewed here.

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“…NAD + may also have a protective role in the aging vasculature, as NMN treatment of old mice improved endothelial relaxation in arteries and reduced artery stiffness 60 . Treatment with a PARP1 inhibitor in a diabetes-induced vascular dysfunction rat model was shown to prevent endothelial dysfunction and inflammation, although NAD + levels were not explicitly investigated 87 . Targeting detrimental changes to the endothelium in aging with SIRT1 activators or NAD + boosters shows promise as an area of focus for treating age-related vascular dysfunction and arterial stiffening.…”

Section: Sirtuins and Nad+ In Age-related Cardiovascular And Metabolimentioning

confidence: 99%

Sirtuins and NAD ⁺ in the Development and Treatment of Metabolic and Cardiovascular Diseases

Kane

Sinclair

2018

Circulation Research

339

270

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The sirtuin family of nicotinamide adenine dinucleotide (NAD+)-dependent deacylases (SIRT1–7) are thought to be responsible, in large part, for the cardiometabolic benefits of lean diets and exercise and when upregulated can delay key aspects of aging. SIRT1, for example, protects against a decline in vascular endothelial function, metabolic syndrome, ischemia-reperfusion (IR) injury, obesity and cardiomyopathy, and SIRT3 is protective against dyslipidemia and IR injury. With increasing age, however, NAD+ levels and sirtuin activity steadily decrease and the decline is further exacerbated by obesity and sedentary lifestyles. Activation of sirtuins or NAD+ repletion induces angiogenesis, insulin sensitivity and other health benefits in a wide range of age-related cardiovascular and metabolic disease models. Human clinical trials testing agents that activate SIRT1 or boost NAD+ levels are in progress and show promise in their ability to improve the health of cardiovascular and metabolic disease patients.

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PARP-1 inhibition alleviates diabetic cardiac complications in experimental animals

Cited by 32 publications

References 47 publications

Association of Methylation Signals With Incident Coronary Heart Disease in an Epigenome-Wide Assessment of Circulating Tumor Necrosis Factor α

Association of Methylation Signals With Incident Coronary Heart Disease in an Epigenome-Wide Assessment of Circulating Tumor Necrosis Factor α

Association of Glycemic Indices (Hyperglycemia, Glucose Variability, and Hypoglycemia) with Oxidative Stress and Diabetic Complications

Sirtuins and NAD ⁺ in the Development and Treatment of Metabolic and Cardiovascular Diseases

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PARP-1 inhibition alleviates diabetic cardiac complications in experimental animals

Cited by 32 publications

References 47 publications

Association of Methylation Signals With Incident Coronary Heart Disease in an Epigenome-Wide Assessment of Circulating Tumor Necrosis Factor α

Association of Methylation Signals With Incident Coronary Heart Disease in an Epigenome-Wide Assessment of Circulating Tumor Necrosis Factor α

Association of Glycemic Indices (Hyperglycemia, Glucose Variability, and Hypoglycemia) with Oxidative Stress and Diabetic Complications

Sirtuins and NAD + in the Development and Treatment of Metabolic and Cardiovascular Diseases

Contact Info

Product

Resources

About

Sirtuins and NAD ⁺ in the Development and Treatment of Metabolic and Cardiovascular Diseases