ArticleHypoxia (Auckland, N.Z.)2019
Role of pseudohypoxia in the pathogenesis of type 2 diabetes.
Article in Hypoxia (Auckland, N.Z.), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 33 citations in OpenAlex.
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- Investigating the Inhibitory Potential of Flavonoids against Aldose Reductase: Insights from Molecular Docking, Dynamics Simulations, and gmx_MMPBSA Analysis.Current issues in molecular biology · 2024Article
- Biomaterials Designed to Modulate Reactive Oxygen Species for Enhanced Bone Regeneration in Diabetic Conditions.Journal of functional biomaterials · 2024Review
- Nicotinamide N-methyltransferase (NNMT): a novel therapeutic target for metabolic syndrome.Frontiers in pharmacology · 2024Review
- Kidney lipid dysmetabolism and lipid droplet accumulation in chronic kidney disease.Nature reviews. Nephrology · 2023Review
- Crabtree effect in kidney proximal tubule cells via late-stage glycolytic intermediates.iScience · 2023Article
- Multi-omics signatures in new-onset diabetes predict metabolic response to dietary inulin: findings from an observational study followed by an interventional trial.Nutrition & diabetes · 2023Observational
- Functions of the aryl hydrocarbon receptor (AHR) beyond the canonical AHR/ARNT signaling pathway.Biochemical pharmacology · 2023Review
- TheInternational journal of molecular sciences · 2022Article
- Cancer heterogeneity and metastasis: life at the edge.Clinical & experimental metastasis · 2022Review
- Identification of a novel association for the WWOX/HIF1A axis with gestational diabetes mellitus (GDM).PeerJ · 2021Article
- Pyruvate-Enriched Oral Rehydration Solution Improves Glucometabolic Disorders in the Kidneys of DiabeticJournal of diabetes research · 2020Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 2 countries.
Funding
Abstract
Type 2 diabetes is caused by persistent high blood glucose, which is known as diabetic hyperglycemia. This hyperglycemic situation, when not controlled, can overproduce NADH and lower nicotinamide adenine dinucleotide (NAD), thereby creating NADH/NAD redox imbalance and leading to cellular pseudohypoxia. In this review, we discussed two major enzymatic systems that are activated by diabetic hyperglycemia and are involved in creation of this pseudohypoxic condition. One system is aldose reductase in the polyol pathway, and the other is poly (ADP ribose) polymerase. While aldose reductase drives overproduction of NADH, PARP could in contrast deplete NAD. Therefore, activation of the two pathways underlies the major mechanisms of NADH/NAD redox imbalance and diabetic pseudohypoxia. Consequently, reductive stress occurs, followed by oxidative stress and eventual cell death and tissue dysfunction. Additionally, fructose formed in the polyol pathway can also cause metabolic syndrome such as hypertension and nonalcoholic fatty liver disease. Moreover, pseudohypoxia can also lower sirtuin protein contents and induce protein acetylation which can impair protein function. Finally, we discussed the possibility of using nicotinamide riboside, an NAD precursor, as a promising therapeutic agent for restoring NADH/NAD redox balance and for preventing the occurrence of diabetic pseudohypoxia.
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