ArticlePloS one2021
Effect of NAD+ boosting on kidney ischemia-reperfusion injury.
Article in PloS one, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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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
34 citing papers in PubMed, 35 citations in OpenAlex.
- Pharmacological activation of SIRT1 alleviates sepsis-associated acute kidney injury by improving renal mitochondrial energy metabolism.Renal failure · 2026Article
- Traditional Chinese Medicine Formulas in Delaying Aging: From Theoretical Foundations to Molecular Mechanisms and Translational Perspectives.Journal of cellular and molecular medicine · 2026Review
- Circadian Influences on Chronic Kidney Disease Progression: Molecular Signaling Pathways of Melatonin and Their Therapeutic Potential.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Chronic Kidney Disease and Cellular Senescence.International journal of molecular sciences · 2026Review
- Integrating metabolomics and machine learning with in silico analysis to identify early biomarkers and molecular interactions in sepsis-associated acute kidney injury.Scientific reports · 2026Article
- The Influence of Sex and Hormones on Organelle Stress in Kidney Injury: Insights from Preclinical Models.Biology · 2026Review
- Article
- Attenuating Ischemia and Reperfusion Injury Using NADTransplantation direct · 2026Article
- Prediction of severe sepsis-associated acute kidney injury incorporating immune-inflammatory profiles: development and validation of a machine learning model in a multicenter prospective cohort study.Frontiers in immunology · 2026Article
- Cellular senescence in renal ischemia-reperfusion injury.Chinese medical journal · 2025Review
- NADTrends in molecular medicine · 2025Review
- Long-Term Functional and Structural Renoprotection After Experimental Acute Kidney Injury in Subclinical Chronic Kidney Disease In Vivo.International journal of molecular sciences · 2025Article
- Nicotinamide Riboside: A Promising Treatment for Type 1 Cardiorenal Syndrome in Myocardial Infarction-Induced Acute Kidney Injury by Upregulating Nicotinamide Phosphoribosyltransferase-Mediated Nicotinamide Dinucleotide Levels.Journal of the American Heart Association · 2025Article
- Acetylation in renal physiology and pathophysiology.Frontiers in pharmacology · 2025Review
- NADCell communication and signaling : CCS · 2024Review
- NAD deficiency contributes to progressive kidney disease in HIV-nephropathy mice.American journal of physiology. Renal physiology · 2024Article
- The Role of Mitochondrial Sirtuins (SIRT3, SIRT4 and SIRT5) in Renal Cell Metabolism: Implication for Kidney Diseases.International journal of molecular sciences · 2024Review
- Comprehensive overview of the role of mitochondrial dysfunction in the pathogenesis of acute kidney ischemia-reperfusion injury: a narrative review.Journal of Yeungnam medical science · 2024Article
- Roles of NADCold Spring Harbor perspectives in medicine · 2024Review
- NAD metabolism: Role in senescence regulation and aging.Aging cell · 2024Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute kidney injury (AKI) is associated with a very high mortality and an increased risk for progression to chronic kidney disease (CKD). Ischemia-reperfusion injury (IRI) is a model for AKI, which results in tubular damage, dysfunction of the mitochondria and autophagy, and in decreased cellular nicotinamide adenine dinucleotide (NAD+) with progressing fibrosis resulting in CKD. NAD+ is a co-enzyme for several proteins, including the NAD+ dependent sirtuins. NAD+ augmentation, e.g. by use of its precursor nicotinamide riboside (NR), improves mitochondrial homeostasis and organismal metabolism in many species. In the present investigation the effects of prophylactic administration of NR on IRI-induced AKI were studied in the rat. Bilateral IRI reduced kidney tissue NAD+, caused tubular damage, reduced α-Klotho (klotho), and altered autophagy flux. AKI initiated progression to CKD, as shown by induced profibrotic Periostin (postn) and Inhibin subunit beta-A, (activin A / Inhba), both 24 hours and 14 days after surgery. NR restored tissue NAD+ to that of the sham group, increased autophagy (reduced p62) and sirtuin1 (Sirt1) but did not ameliorate renal tubular damage and profibrotic genes in the 24 hours and 14 days IRI models. AKI induced NAD+ depletion and impaired autophagy, while augmentation of NAD+ by NR restored tissue NAD+ and increased autophagy, possibly serving as a protective response. However, prophylactic administration of NR did not ameliorate tubular damage of the IRI rats nor rescued the initiation of fibrosis in the long-term AKI to CKD model, which is a pivotal event in CKD pathogenesis.
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