High-glucose diets induce mitochondrial dysfunction in Caenorhabditis elegans

Alcántar‐Fernández, Jonathan; González-Maciel, Angélica; Reynoso-Robles, Rafael; Andrade, Martha Elva Pérez; Hernández-Vázquez, Alain; Velázquez-Arellano, Antonio; Miranda-Ríos, Juan

doi:10.1371/journal.pone.0226652

Cited by 34 publications

(26 citation statements)

References 75 publications

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“…Enhanced ROS in response to high glucose interferes with the mitochondrial electron transport chain, which increases the oxidation of coenzyme Q, thus forming peroxides. These peroxides react with nitrous oxide to form peroxynitrite (ONOO − ), which leads to mitochondrial protein dysfunction, lipid oxidation, and DNA modification, eventually leading to cell apoptosis [ 136 ].…”

Section: High Glucosementioning

confidence: 99%

Natural Antioxidants Improve the Vulnerability of Cardiomyocytes and Vascular Endothelial Cells under Stress Conditions: A Focus on Mitochondrial Quality Control

Chang

Zhao

Zhang

et al. 2021

Oxidative Medicine and Cellular Longevity

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Cardiovascular disease has become one of the main causes of human death. In addition, many cardiovascular diseases are accompanied by a series of irreversible damages that lead to organ and vascular complications. In recent years, the potential therapeutic strategy of natural antioxidants in the treatment of cardiovascular diseases through mitochondrial quality control has received extensive attention. Mitochondria are the main site of energy metabolism in eukaryotic cells, including myocardial and vascular endothelial cells. Mitochondrial quality control processes ensure normal activities of mitochondria and cells by maintaining stable mitochondrial quantity and quality, thus protecting myocardial and endothelial cells against stress. Various stresses can affect mitochondrial morphology and function. Natural antioxidants extracted from plants and natural medicines are becoming increasingly common in the clinical treatment of diseases, especially in the treatment of cardiovascular diseases. Natural antioxidants can effectively protect myocardial and endothelial cells from stress-induced injury by regulating mitochondrial quality control, and their safety and effectiveness have been preliminarily verified. This review summarises the damage mechanisms of various stresses in cardiomyocytes and vascular endothelial cells and the mechanisms of natural antioxidants in improving the vulnerability of these cell types to stress by regulating mitochondrial quality control. This review is aimed at paving the way for novel treatments for cardiovascular diseases and the development of natural antioxidant drugs.

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Section: High Glucosementioning

confidence: 99%

Natural Antioxidants Improve the Vulnerability of Cardiomyocytes and Vascular Endothelial Cells under Stress Conditions: A Focus on Mitochondrial Quality Control

Chang

Zhao

Zhang

et al. 2021

Oxidative Medicine and Cellular Longevity

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“…This hypothesis could be readily tested by determining if knockdown of acly-1 or acs-19 /ACSS2 largely prevents metabolite-mediated lifespan extension. Although glucose supplementation to young adult worms decreases lifespan in part due to mitochondrial dysfunction [ 420 ], glucose supplementation only during larval development [ 421 ] or only during the post-reproductive period [ 422 ] extends lifespan, which could be mediated by increased nucleocytoplasmic acetyl-CoA levels and histone acetylation.…”

Section: Experiments Using C Elegans Suggest That Increased Acetyl-coa Synthesis Stimulates Longevitymentioning

confidence: 99%

Acetyl-CoA Metabolism and Histone Acetylation in the Regulation of Aging and Lifespan

Bradshaw

2021

Antioxidants

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Acetyl-CoA is a metabolite at the crossroads of central metabolism and the substrate of histone acetyltransferases regulating gene expression. In many tissues fasting or lifespan extending calorie restriction (CR) decreases glucose-derived metabolic flux through ATP-citrate lyase (ACLY) to reduce cytoplasmic acetyl-CoA levels to decrease activity of the p300 histone acetyltransferase (HAT) stimulating pro-longevity autophagy. Because of this, compounds that decrease cytoplasmic acetyl-CoA have been described as CR mimetics. But few authors have highlighted the potential longevity promoting roles of nuclear acetyl-CoA. For example, increasing nuclear acetyl-CoA levels increases histone acetylation and administration of class I histone deacetylase (HDAC) inhibitors increases longevity through increased histone acetylation. Therefore, increased nuclear acetyl-CoA likely plays an important role in promoting longevity. Although cytoplasmic acetyl-CoA synthetase 2 (ACSS2) promotes aging by decreasing autophagy in some peripheral tissues, increased glial AMPK activity or neuronal differentiation can stimulate ACSS2 nuclear translocation and chromatin association. ACSS2 nuclear translocation can result in increased activity of CREB binding protein (CBP), p300/CBP-associated factor (PCAF), and other HATs to increase histone acetylation on the promoter of neuroprotective genes including transcription factor EB (TFEB) target genes resulting in increased lysosomal biogenesis and autophagy. Much of what is known regarding acetyl-CoA metabolism and aging has come from pioneering studies with yeast, fruit flies, and nematodes. These studies have identified evolutionary conserved roles for histone acetylation in promoting longevity. Future studies should focus on the role of nuclear acetyl-CoA and histone acetylation in the control of hypothalamic inflammation, an important driver of organismal aging.

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“…Furthermore, IL-6 is thought to play an important role in atherosclerosis in T2D [56]. We show an increase in mtROS production in leukocytes from T2D patients that was more pronounced in subjects with HbA 1c > 6.5%, suggesting that leukocyte mitochondrial function can be altered during chronic hyperglycemia [70,[72][73][74]. Other studies in the field have suggested that good glycemic control reduces ROS production [57,75,76].…”

Section: Discussionmentioning

confidence: 63%

Association between Proinflammatory Markers, Leukocyte–Endothelium Interactions, and Carotid Intima–Media Thickness in Type 2 Diabetes: Role of Glycemic Control

Iannantuoni

Abad-Jiménez

Canet

et al. 2020

JCM

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Glycated hemoglobin monitorization could be a tool for maintaining type 2 diabetes (T2D) under control and delaying the appearance of cardiovascular events. This cross-sectional study was designed to assess the role of glycemic control in modulating early-stage markers of cardiovascular complications. One hundred and eight healthy controls and 161 type 2 diabetic patients were recruited and distributed according to their glycemic control, setting the threshold at 6.5% (good control). Biochemical and anthropometrical parameters were registered during the initial visit, and peripheral blood was extracted to obtain polymorphonuclear cells and analyze inflammatory markers, adhesion molecules, leukocyte–endothelium interactions, and carotid intima–media thickness. Correlations between these parameters were explored. We found that inflammatory markers and adhesion molecules were augmented in type 2 diabetic subjects with poor glycemic control. Polymorphonuclear leukocytes interacted more with the endothelium in the diabetic population, and even more significantly in the poorly controlled subjects. In parallel, carotid intima–media thickness was also increased in the diabetic population, and the difference was greater among poorly controlled subjects. Finally, correlation measurement revealed that carotid intima–media thickness was related to glycemic control and lipid metabolism in diabetic patients. Our results suggest that glycemic control delays the onset of cardiovascular comorbidities in diabetic subjects.

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High-glucose diets induce mitochondrial dysfunction in Caenorhabditis elegans

Cited by 34 publications

References 75 publications

Natural Antioxidants Improve the Vulnerability of Cardiomyocytes and Vascular Endothelial Cells under Stress Conditions: A Focus on Mitochondrial Quality Control

Natural Antioxidants Improve the Vulnerability of Cardiomyocytes and Vascular Endothelial Cells under Stress Conditions: A Focus on Mitochondrial Quality Control

Acetyl-CoA Metabolism and Histone Acetylation in the Regulation of Aging and Lifespan

Association between Proinflammatory Markers, Leukocyte–Endothelium Interactions, and Carotid Intima–Media Thickness in Type 2 Diabetes: Role of Glycemic Control

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