Mitochondrial Dysfunction, Oxidative Stress, and Therapeutic Strategies in Diabetes, Obesity, and Cardiovascular Disease

Cojocaru, Karina-Alexandra; Luchian, Ionuț; Goriuc, Ancuța; Antoci, Lucian-Mihai; Ciobanu, Cristian-Gabriel; Popescu, Roxana; Vlad, Cristiana-Elena; Blaj, Mihaela; Foia, Liliana

doi:10.3390/antiox12030658

Cited by 36 publications

(25 citation statements)

References 141 publications

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“…In patients with type 2 diabetes, insulin resistance is induced by changes in OXPHOS levels, reduced NADH oxidoreductase and citrate synthase activity ( 87 ). In contrast, data on changes in metabolic reprogramming in patients with GDM are still limited.…”

Section: Gestational Diabetes and Metabolic Reprogrammingmentioning

confidence: 99%

Recent progress in metabolic reprogramming in gestational diabetes mellitus: a review

Xie,

Lin,

Xie

et al. 2024

Front. Endocrinol.

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Gestational diabetes mellitus is a prevalent metabolic disease that can impact the normal course of pregnancy and delivery, leading to adverse outcomes for both mother and child. Its pathogenesis is complex and involves various factors, such as insulin resistance and β-cell dysfunction. Metabolic reprogramming, which involves mitochondrial oxidative phosphorylation and glycolysis, is crucial for maintaining human metabolic balance and is involved in the pathogenesis and progression of gestational diabetes mellitus. However, research on the link and metabolic pathways between metabolic reprogramming and gestational diabetes mellitus is limited. Therefore, we reviewed the relationship between metabolic reprogramming and gestational diabetes mellitus to provide new therapeutic strategies for maternal health during pregnancy and reduce the risk of developing gestational diabetes mellitus.

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Section: Gestational Diabetes and Metabolic Reprogrammingmentioning

confidence: 99%

Recent progress in metabolic reprogramming in gestational diabetes mellitus: a review

Xie,

Lin,

Xie

et al. 2024

Front. Endocrinol.

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“…An imbalance between the production of reactive nitrogen species (RNS) and reactive oxygen species (ROS), together with an absent or poor antioxidant system, leads to oxidative stress [32]. ROS can be of exogenous or endogenous origin, while the mitochondrial respiratory chain is the main endogenous source of ROS [33]. During the early stages of atherosclerotic lesion formation, enzymes such as nitric oxide synthase and xanthine oxidase contribute to oxidative stress [34], which is also associated with local inflammation, endothelial dysfunction, SMC proliferation, and plaque formation [35].…”

Section: Role Of Oxidative Stress In Atherosclerosismentioning

confidence: 99%

The Role of Punicalagin and Its Metabolites in Atherosclerosis and Risk Factors Associated with the Disease

Alalawi,

Albalawi,

Ramji

2023

IJMS

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Atherosclerotic cardiovascular disease (ACVD) is the leading cause of death worldwide. Although current therapies, such as statins, have led to a marked reduction in morbidity and mortality from ACVD, they are associated with considerable residual risk for the disease together with various adverse side effects. Natural compounds are generally well-tolerated; a major recent goal has been to harness their full potential in the prevention and treatment of ACVD, either alone or together with existing pharmacotherapies. Punicalagin (PC) is the main polyphenol present in pomegranates and pomegranate juice and demonstrates many beneficial actions, including anti-inflammatory, antioxidant, and anti-atherogenic properties. The objective of this review is to inform on our current understanding of the pathogenesis of ACVD and the potential mechanisms underlying the beneficial actions of PC and its metabolites in the disease, including the attenuation of dyslipidemia, oxidative stress, endothelial cell dysfunction, foam cell formation, and inflammation mediated by cytokines and immune cells together with the regulation of proliferation and migration of vascular smooth muscle cells. Some of the anti-inflammatory and antioxidant properties of PC and its metabolites are due to their strong radical-scavenging activities. PC and its metabolites also inhibit the risk factors of atherosclerosis, including hyperlipidemia, diabetes mellitus, inflammation, hypertension, obesity, and non-alcoholic fatty liver disease. Despite the promising findings that have emerged from numerous in vitro, in vivo, and clinical studies, deeper mechanistic insights and large clinical trials are required to harness the full potential of PC and its metabolites in the prevention and treatment of ACVD.

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“…Oxidative stress is an imbalance between increased prooxidants and insufficient antioxidants that occurs when excessive production of reactive oxygen and nitrogen species (ROS/RNS) such as hydroxyl radical (HO ⋅ ), superoxide anion (O 2 ⋅− ), hydrogen peroxide (H 2 O 2 ), nitric oxide (NO ⋅ ), nitroxyl anion (NO − ), and peroxynitrite (NOOO ⋅ ). Oxidative stress oxidized lipids, proteins, DNA and damaged cell functions and thus it is implicated in the pathogenesis of various diseases 14 .…”

Section: Introductionmentioning

confidence: 99%

High methionine diet mediated oxidative stress and proteasome impairment causes toxicity in liver

Derouiche,

Djemil,

Sebihi

et al. 2024

Sci Rep

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Methionine (Met) rich diet inducing oxidative stress is reported to alter many organs. Proteasome as a regulator of oxidative stress can be targeted. This study was performed to investigate if excessive methionine supplementation causes hepatotoxicity related to proteasome dysfunction under endogenous oxidative stress in rats. Male Wistar albino rats (n = 16) were divided into controls and treated groups. The treated rats (n = 08) received orally l-methionine (1 g/kg/day) for 21 days. Total homocysteine (tHcy), total oxidant status (TOS), total antioxidant status (TAS), hepatic enzymes levels: aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH), alkaline phosphatase (ALP), with total bilirubin (TBil), albumin (Alb), and C-reactive protein (CRP) were determined in plasma by biochemical assays. Liver supernatants were used for malondialdehyde (MDA), protein carbonyls (PC), glutathione (GSH), catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx), 20S proteasome activities and their subunits expression, tumor necrosis factor-α (TNF-α), and interleukin 6 (IL-6) evaluation by appropriate methods and light microscopy for liver histological examination. Methionine treatment increased homocysteine, TOS, oxidative stress index (OSI), MDA and PC but decreased TAS, GSH, CAT, SOD, GPx with the 20S proteasome activities and their β subunits expression. Liver proteins: AST, ALT, LDH, ALP, TBil and CRP were increased but Alb was decreased. Liver histology was also altered. An increase in liver TNF-α and IL-6 levels were observed. These findings indicated that methionine supplementation associated oxidative stress and proteasome dysfunction, caused hepatotoxicity and inflammation in rat. Further investigations should be to better understand the relation between methionine, oxidative stress, proteasome, and liver injuries.

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Mitochondrial Dysfunction, Oxidative Stress, and Therapeutic Strategies in Diabetes, Obesity, and Cardiovascular Disease

Cited by 36 publications

References 141 publications

Recent progress in metabolic reprogramming in gestational diabetes mellitus: a review

Recent progress in metabolic reprogramming in gestational diabetes mellitus: a review

The Role of Punicalagin and Its Metabolites in Atherosclerosis and Risk Factors Associated with the Disease

High methionine diet mediated oxidative stress and proteasome impairment causes toxicity in liver

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