ArticleExperimental and therapeutic medicine2018
Insulin alleviates mitochondrial oxidative stress involving upregulation of superoxide dismutase 2 and uncoupling protein 2 in septic acute kidney injury.
Article in Experimental and therapeutic medicine, 2018. 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, 31 citations in OpenAlex.
- Mitochondrial membrane potential and delayed graft function following kidney transplantation.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2019Trial
- Mitochondrial complex I in focus: mechanisms and therapeutic strategies of urinary system diseases.Frontiers in physiology · 2026Review
- Protective effects of insulin on dry eye syndrome via TLR4/NF-κB pathway: based on network pharmacology andFrontiers in pharmacology · 2024Article
- MicroRNAs in septic acute kidney injury.Burns & trauma · 2023Article
- Benefits and risks of essential trace elements in chronic kidney disease: a narrative review.Annals of translational medicine · 2022Review
- NEAT1 Confers Radioresistance to Hepatocellular Carcinoma Cells by Inducing PINK1/Parkin-Mediated Mitophagy.International journal of molecular sciences · 2022Article
- Bioinspired copper single-atom nanozyme as a superoxide dismutase-like antioxidant for sepsis treatment.Exploration (Beijing, China) · 2022Article
- Potential roles of mitochondrial cofactors in the adjuvant mitigation of proinflammatory acute infections, as in the case of sepsis and COVID-19 pneumonia.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2021Review
- The Protective Effects of Perindopril Against Acute Kidney Damage Caused by Septic Shock.Inflammation · 2021Article
- Article
- Manganese Superoxide Dismutase Dysfunction and the Pathogenesis of Kidney Disease.Frontiers in physiology · 2020Review
- Acute kidney injury from sepsis: current concepts, epidemiology, pathophysiology, prevention and treatment.Kidney international · 2019Review
- UCP2 silencing aggravates mitochondrial dysfunction in astrocytes under septic conditions.Molecular medicine reports · 2019Article
- Biomarkers in Stress Related Diseases/Disorders: Diagnostic, Prognostic, and Therapeutic Values.Frontiers in molecular biosciences · 2019Review
- Chronic Insulin Infusion Down-Regulates Circulating and Urinary Nitric Oxide (NO) Levels Despite Molecular Changes in the Kidney Predicting Greater Endothelial NO Synthase Activity in Mice.International journal of molecular sciences · 2018Article
- Time course of liver mitochondrial function and intrinsic changes in oxidative phosphorylation in a rat model of sepsis.Intensive care medicine experimental · 2018Article
- Role of Mitochondrial Oxidative Stress in Sepsis.Acute and critical care · 2018Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aim of the present study was to explore the effects and mechanisms of insulin on mitochondrial oxidative stress in septic acute kidney injury (AKI). Male Sprague Dawley rats were divided randomly into four groups: Control group, sham surgery group, cecal ligation and puncture (CLP) group, and CLP plus insulin group. Blood specimens and kidney tissues were obtained at 12 and 24 h after surgery as separate experiments. Analyses of histology and indicators of renal injury [blood urea nitrogen (BUN) and serum creatinine (CRE) and neutrophil gelatinase-associated lipocalin (NGAL)], mitochondrial function [adenosine triphosphate (ATP) and mitochondrial membrane potential (MMP)], oxidative stress [inducible nitric oxide synthase (iNOS), reactive oxygen species (ROS) and nitric oxide (NO)], endogenous antioxidant systems [superoxide dismutase (SOD) and glutathione (GSH)] as well as the expression of uncoupling protein (UCP), PINK1 protein (a major mediator of mitophagy), PGC1α protein (a major regulator of mitochondrial biogenesis) were performed. Compared with CLP group, the CLP plus insulin group had milder histological damage, higher levels of ATP and MMP as well as lower levels of BUN, serum CRE and NGAL, intrarenal iNOS, mitochondrial ROS and total NO. Moreover, the CLP plus insulin group demonstrated increased expression of SOD2 and UCP2. In contrast, insulin administration suppressed mitophagy meanwhile did not upregulate total GSH and induce mitochondrial biogenesis following CLP. These findings indicated that the upregulation of SOD2 and UCP2 may be involved in insulin protecting against mitochondrial oxidative stress in septic AKI.
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Registered trials
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