ReviewDiabetes, metabolic syndrome and obesity : targets and therapy2016
Sources and implications of NADH/NAD(+) redox imbalance in diabetes and its complications.
Review in Diabetes, metabolic syndrome and obesity : targets and therapy, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 121 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
121 citing papers in PubMed, 196 citations in OpenAlex.
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- The Reductive Stress Nexus: Integrated Pathways of Metabolic Dysregulation, Senescence and Blood-Brain Barrier Failure in Neurodegenerative Disease and Brain Aging.Cell biochemistry and biophysics · 2026Review
- Divergent Atrial Transcriptomic Signatures in Diabetic and Nondiabetic Atrial Fibrillation.Journal of arrhythmia · 2026Article
- TRIM38 alleviates the pathogenesis of diabetic nephropathy by suppressing NF-κB activation via inducing RIPK1 degradation.Journal of physiology and biochemistry · 2026Article
- pH and Glucose Dual-Responsive Hybrid Polymeric Smart Insulin Carrier for Diabetes Treatment.Polymers · 2026Article
- Dysregulation of the glycolysis-mitochondrial metabolism axis in osteoarthritis: mechanisms and therapeutic implications.Journal of orthopaedic translation · 2026Review
- Bi-Polar Bioenergetic Intervention via a Pathology Self-Adaptive Single-Atom Nanocatalyst for Diabetic Tumor Postoperative Management.Nano-micro letters · 2026Article
- NSDHL as a regulator of lipid peroxidation and ER stress-mediated apoptosis in ovarian cancer.Biology direct · 2026Article
- Oxidative Stress in Diabetic Cardiomyopathy: Molecular Mechanisms and Emerging Therapeutic Targets.Biomolecules · 2026Review
- Renoprotection by 5-Methoxytryptophan in Kidney Disease.Biomolecules · 2026Review
- Modeling tissue-specific Drosophila metabolism identifies high sugar diet-induced metabolic dysregulation in muscle at reaction and pathway levels.Nature communications · 2026Article
- Reversible phase dynamics of PsAF5 regulate mitophagy to balance redox levels inScience advances · 2026Article
- Sex-specific differences in vascular circulation and metabolic regulation associated with aging and cardiovascular health problems.Frontiers in aging · 2026Article
- Intravenous infusion of nicotinamide adenine dinucleotide (NADFrontiers in aging · 2026Article
- Semaphorin3A Rewires CD4International journal of molecular sciences · 2025Article
- Reductive stress: The key pathway in metabolic disorders induced by overnutrition.Journal of advanced research · 2025Review
- Human iPSC-derived salivary gland organoids model diabetic salivary gland dysfunction.bioRxiv : the preprint server for biology · 2025Article
- Combined nicotinamide riboside and magnesium-l-theanine protects against chronic stress-induced gut-liver injury by modulating NAD⁺ and metabolic pathways.Molecular biology reports · 2025Article
- Respiration defects limit serine synthesis required for lung cancer growth and survival.Nature communications · 2025Article
61 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
NAD(+) is a fundamental molecule in metabolism and redox signaling. In diabetes and its complications, the balance between NADH and NAD(+) can be severely perturbed. On one hand, NADH is overproduced due to influx of hyperglycemia to the glycolytic and Krebs cycle pathways and activation of the polyol pathway. On the other hand, NAD(+) can be diminished or depleted by overactivation of poly ADP ribose polymerase that uses NAD(+) as its substrate. Moreover, sirtuins, another class of enzymes that also use NAD(+) as their substrate for catalyzing protein deacetylation reactions, can also affect cellular content of NAD(+). Impairment of NAD(+) regeneration enzymes such as lactate dehydrogenase in erythrocytes and complex I in mitochondria can also contribute to NADH accumulation and NAD(+) deficiency. The consequence of NADH/NAD(+) redox imbalance is initially reductive stress that eventually leads to oxidative stress and oxidative damage to macromolecules, including DNA, lipids, and proteins. Accordingly, redox imbalance-triggered oxidative damage has been thought to be a major factor contributing to the development of diabetes and its complications. Future studies on restoring NADH/NAD(+) redox balance could provide further insights into design of novel antidiabetic strategies.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.