ArticleRedox biology2017
Probucol ameliorates renal injury in diabetic nephropathy by inhibiting the expression of the redox enzyme p66Shc.
Article in Redox biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 27 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
27 citing papers in PubMed, 56 citations in OpenAlex.
- Probucol inhibits palmitic acid-mediated renal calcium oxalate stone formation by targeting KLF5-PPARγ axis-mediated lipotoxicity.Journal of pharmaceutical analysis · 2026Article
- Tubular Injury in Diabetic Kidney Disease: Early Diagnosis and Intervention Strategies.Diabetes/metabolism research and reviews · 2025Review
- Inhibition of AMPKα Pathway by Podocyte GOLM1 Exacerbates Diabetic Nephrology in Mice.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Metformin attenuates diabetic osteoporosis by suppressing ferroptosis via the AMPK/Nrf2 pathway.Frontiers in pharmacology · 2025Article
- Beneficial effects of food-medicine homologous herbs for patients with diabetic kidney disease.Frontiers in immunology · 2025Review
- SAHA inhibits lung fibroblast activation by increasing p66Shc expression epigenetically.Aging medicine (Milton (N.S.W)) · 2024Article
- Sirtuins in kidney diseases: potential mechanism and therapeutic targets.Cell communication and signaling : CCS · 2024Review
- SIRT1-SIRT7 in Diabetic Kidney Disease: Biological Functions and Molecular Mechanisms.Frontiers in endocrinology · 2022Review
- The Role of p66Shc in Diabetes: A Comprehensive Review from Bench to Bedside.Journal of diabetes research · 2022Review
- circ_000166/miR-296 Aggravates the Process of Diabetic Renal Fibrosis by Regulating the SGLT2 Signaling Pathway in Renal Tubular Epithelial Cells.Disease markers · 2022Article
- Review
- A Review on Recent Advancement on Age-Related Hearing Loss: The Applications of Nanotechnology, Drug Pharmacology, and Biotechnology.Pharmaceutics · 2021Review
- RvD1 Attenuated Susceptibility to Ischemic AKI in Diabetes by Downregulating Nuclear Factor-κ B Signal and Inhibiting Apoptosis.Frontiers in physiology · 2021Article
- LncRNA MALAT1 promoted high glucose-induced pyroptosis of renal tubular epithelial cell by sponging miR-30c targeting for NLRP3.The Kaohsiung journal of medical sciences · 2020Article
- Epigenetic Regulation Associated With Sirtuin 1 in Complications of Diabetes Mellitus.Frontiers in endocrinology · 2020Review
- Probucol Prevents Diabetes-Induced Retinal Neuronal Degeneration through Upregulating Nrf2.BioMed research international · 2020Article
- Probucol promotes high glucose-induced proliferation and inhibits apoptosis by reducing reactive oxygen species generation in Müller cells.International ophthalmology · 2019Article
- Inhibition of STAT3 in tubular epithelial cells prevents kidney fibrosis and nephropathy in STZ-induced diabetic mice.Cell death & disease · 2019Article
- STC-1 ameliorates renal injury in diabetic nephropathy by inhibiting the expression of BNIP3 through the AMPK/SIRT3 pathway.Laboratory investigation; a journal of technical methods and pathology · 2019Article
- DsbA-L ameliorates high glucose induced tubular damage through maintaining MAM integrity.EBioMedicine · 2019Article
Corrections and comments
- Erratum issued
- Retracted
Authors and funding
14 authors at 4 institutions in 2 countries.
Funding
Abstract
aimsProbucol is an anti-hyperlipidemic agent and a potent antioxidant drug that can delay progression of diabetic nephropathy (DN) and reverses renal oxidative stress in diabetic animal models; however, the mechanisms underlying these effects remain unclear. p66Shc is a newly recognized mediator of mitochondrial ROS production in renal cells under high-glucose (HG) ambience. We previously showed that p66Shc can serve as a biomarker for renal oxidative injury in DN patients and that p66Shc up-regulation is correlated with renal damage in vivo and in vitro. Here, we determined whether probucol ameliorates renal injury in DN by inhibiting p66Shc expression.
resultsWe found that the expression of SIRT1, Ac-H3 and p66Shc in kidneys of DN patients was altered. Also, probucol reduced the levels of serum creatinine, urine protein and LDL-c and attenuated renal oxidative injury and fibrosis in STZ induced diabetic mice. In addition, probucol reversed p-AMPK, SIRT1, Ac-H3 and p66Shc expression. Correlation analyses showed that p66Shc expression was correlated with p-AMPK and Sirt1 expression and severity of renal injury. In vitro pretreatment of HK-2 cells with p-AMPK and SIRT1 siRNA negated the beneficial effects of probucol. Furthermore, we noted that probucol activates p-AMPK and Sirt1 and inhibits p66shc mRNA transcription by facilitating the binding of Sirt1 to the p66Shc promoter and modulation of Ac-H3 expression in HK-2 cells under HG ambience. INNOVATION AND
conclusionOur results suggest for the first time that probucol ameliorates renal damage in DN by epigenetically suppressing p66Shc expression via the AMPK-SIRT1-AcH3 pathway.
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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.