ArticleEndocrinology2009
Poly(Adenosine 5'-diphosphate-ribose) polymerase inhibition counteracts multiple manifestations of experimental type 1 diabetic nephropathy.
Article in Endocrinology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 27 citations in OpenAlex.
- PARP-1 inhibition attenuates tumor pathology in a novel murine model of diabetes-associated colitis-induced colorectal cancer.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Identification and validation of parthanatos-related genes in end-stage renal disease.Renal failure · 2025Article
- Molecular Mechanisms of Parthanatos and Its Role in Diverse Diseases.International journal of molecular sciences · 2022Review
- 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
- Evaluation of neonatal streptozotocin induced diabetic rat model for the development of cataract.Oxidative medicine and cellular longevity · 2014Article
- Prediabetic nephropathy as an early consequence of the high-calorie/high-fat diet: relation to oxidative stress.Endocrinology · 2012Article
- Poly(ADP-ribose)polymerase inhibition counteracts renal hypertrophy and multiple manifestations of peripheral neuropathy in diabetic Akita mice.International journal of molecular medicine · 2011Article
- PARP inhibition alleviates diabetes-induced systemic oxidative stress and neural tissue 4-hydroxynonenal adduct accumulation: correlation with peripheral nerve function.Free radical biology & medicine · 2011Article
- Poly(ADP-ribose) polymerase-1 inhibition: preclinical and clinical development of synthetic lethality.Molecular medicine (Cambridge, Mass.) · 2011Review
- Peroxynitrite-driven mechanisms in diabetes and insulin resistance - the latest advances.Current medicinal chemistry · 2011Review
- Poly(ADP-ribose) polymerase-1 (PARP-1) gene deficiency alleviates diabetic kidney disease.Biochimica et biophysica acta · 2010Article
- Role of 12/15-lipoxygenase in nitrosative stress and peripheral prediabetic and diabetic neuropathies.Free radical biology & medicine · 2010Article
- New therapeutic and biomarker discovery for peripheral diabetic neuropathy: PARP inhibitor, nitrotyrosine, and tumor necrosis factor-{alpha}.Endocrinology · 2010Article
- Poly(ADP-ribose) polymerase (PARP) inhibition counteracts multiple manifestations of kidney disease in long-term streptozotocin-diabetic rat model.Biochemical pharmacology · 2010Article
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7 authors at 3 institutions in 1 country.
Funding
Abstract
This study was aimed at evaluating the role for poly(ADP-ribose) polymerase (PARP) in early nephropathy associated with type 1 diabetes. Control and streptozotocin-diabetic rats were maintained with or without treatment with one of two structurally unrelated PARP inhibitors, 1,5-isoquinolinediol (ISO) and 10-(4-methyl-piperazin-1-ylmethyl)-2H-7-oxa-1,2-diaza-benzo[de] anthracen-3-one (GPI-15427), at 3 mg/kg(-1) x d(-1) ip and 30 mg/kg(-1) x d(-1), respectively, for 10 wk after the first 2 wk without treatment. PARP activity in the renal cortex was assessed by immunohistochemistry and Western blot analysis of poly(ADP-ribosyl)ated proteins. Variables of diabetic nephropathy in urine and renal cortex were evaluated by ELISA, Western blot analysis, immunohistochemistry, and colorimetry. Urinary albumin excretion was increased about 4-fold in diabetic rats, and this increase was prevented by ISO and GPI-15427. PARP inhibition counteracted diabetes-associated increase in poly(ADP-ribose) immunoreactivities in renal glomeruli and tubuli and poly(ADP-ribosyl)ated protein level. Renal concentrations of TGF-beta(1), vascular endothelial growth factor, endothelin-1, TNF-alpha, monocyte chemoattractant protein-1, lipid peroxidation products, and nitrotyrosine were increased in diabetic rats, and all these changes as well as an increase in urinary TNF-alpha excretion were completely or partially prevented by ISO and GPI-15427. PARP inhibition counteracted diabetes-induced up-regulation of endothelin (B) receptor, podocyte loss, accumulation of collagen-alpha1 (IY), periodic acid-Schiff-positive substances, fibronectin, and advanced glycation end-products in the renal cortex. In conclusion, PARP activation is implicated in multiple changes characteristic for early nephropathy associated with type 1 diabetes. These findings provide rationale for development and further studies of PARP inhibitors and PARP inhibitor-containing combination therapies.
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