ArticleBiochemical pharmacology2010
Poly(ADP-ribose) polymerase (PARP) inhibition counteracts multiple manifestations of kidney disease in long-term streptozotocin-diabetic rat model.
Article in Biochemical pharmacology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 35 citations in OpenAlex.
- LncRNA ENST00000532153.1 alleviates podocyte injury by inhibiting PARP1-mediated PARylation of ATF3 in diabetic kidney disease.Cellular and molecular life sciences : CMLS · 2025Article
- Cell death induced by acute renal injury: a perspective on the contributions of accidental and programmed cell death.American journal of physiology. Renal physiology · 2024Review
- Poly(ADP-ribose) polymerase-1 affects vasopressin-mediated AQP2 expression in collecting duct cells of the kidney.American journal of physiology. Renal physiology · 2024Article
- EDB-FN targeted probes for the surgical navigation, radionuclide imaging, and therapy of thyroid cancer.European journal of nuclear medicine and molecular imaging · 2023Article
- D-ribose: Potential clinical applications in congestive heart failure and diabetes, and its complications (Review).Experimental and therapeutic medicine · 2021Review
- Autophagy Function and Regulation in Kidney Disease.Biomolecules · 2020Review
- Intraperitoneal Administration of Oxygen/Ozone to Rats Reduces the Pancreatic Damage Induced by Streptozotocin.Biology · 2018Article
- PARP inhibition ameliorates nephropathy in an animal model of type 2 diabetes: focus on oxidative stress, inflammation, and fibrosis.Naunyn-Schmiedeberg's archives of pharmacology · 2017Article
- Regulation of necrotic cell death: p53, PARP1 and cyclophilin D-overlapping pathways of regulated necrosis?Cellular and molecular life sciences : CMLS · 2016Review
- Cisplatin induces primary necrosis through poly(ADP-ribose) polymerase 1 activation in kidney proximal tubular cells.Anatomy & cell biology · 2015Article
- Antagonistic crosstalk between SIRT1, PARP-1, and -2 in the regulation of chronic inflammation associated with aging and metabolic diseases.Integrative medicine research · 2014Review
- New insights into the molecular and cellular functions of poly(ADP-ribose) and PARPs.Nature reviews. Molecular cell biology · 2012Review
- On PAR with PARP: cellular stress signaling through poly(ADP-ribose) and PARP-1.Genes & development · 2012Review
- A metabolomic study of low estimated GFR in non-proteinuric type 2 diabetes mellitus.Diabetologia · 2012Article
- Animal models as tools to investigate antidiabetic and anti-inflammatory plants.Evidence-based complementary and alternative medicine : eCAM · 2012Article
- Poly(ADP-ribose) polymerase-1 is a key mediator of cisplatin-induced kidney inflammation and injury.Free radical biology & medicine · 2011Article
- Poly(ADP-ribose)polymerase inhibition counteracts renal hypertrophy and multiple manifestations of peripheral neuropathy in diabetic Akita mice.International journal of molecular medicine · 2011Article
- Why does atorvastatin inhibit renal crystal retention?Urological research · 2011Article
- Preventive effects of benfotiamine in chronic diabetic complications.Journal of diabetes investigation · 2011Article
- Poly(ADP-ribose) polymerase-1 inhibition: preclinical and clinical development of synthetic lethality.Molecular medicine (Cambridge, Mass.) · 2011Review
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Authors and funding
10 authors at 3 institutions in 1 country.
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Abstract
Evidence for the important role for poly(ADP-ribose) polymerase (PARP) in the pathogenesis of diabetic nephropathy is emerging. We previously reported that PARP inhibitors counteract early Type 1 diabetic nephropathy. This study evaluated the role for PARP in kidney disease in long-term Type 1 diabetes. Control and streptozotocin-diabetic rats were maintained with or without treatment with the PARP inhibitor 10-(4-methyl-piperazin-1-ylmethyl)-2H-7-oxa-1,2-diaza-benzo[de] anthracen-3-one (GPI-15,427, Eisai Inc.), 30mgkg(-1)d(-1), for 26 weeks after first 2 weeks without treatment. PARP activity in the renal cortex was assessed by Western blot analysis of poly(ADP-ribosyl)ated proteins. Urinary albumin, isoprostane, and 8-hydroxy-2'-deoxyguanosine excretion, and renal concentrations of transforming growth factor-beta(1), vascular endothelial growth factor, soluble intercellular adhesion molecule-1, fibronectin, and nitrotyrosine were evaluated by ELISA, and urinary creatinine and renal lipid peroxidation products by colorimetric assays. PARP inhibition counteracted diabetes-associated increase in renal cortex poly(ADP-ribosyl)ated protein level. Urinary albumin, isoprostane, and 8-hydroxy-2'-deoxyguanosine excretions and urinary albumin/creatinine ratio were increased in diabetic rats, and all these changes were at least partially prevented by GPI-15,427 treatment. PARP inhibition counteracted diabetes-induced renal transforming growth factor-beta(1), vascular endothelial growth factor, and fibronectin, but not soluble intercellular adhesion molecule-1 and nitrotyrosine, accumulations. Lipid peroxidation product concentrations were indistinguishable among control and diabetic rats maintained with or without GPI-15,427 treatment. In conclusion, PARP activation plays an important role in kidney disease in long-term diabetes. These findings provide rationale for development and further studies of PARP inhibitors and PARP inhibitor-containing combination therapies, for prevention and treatment of diabetic nephropathy.
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