ArticleThe journal of physiological sciences : JPS2015
Poly(ADP-ribose) polymerase 1 activation links ischemic acute kidney injury to interstitial fibrosis.
Article in The journal of physiological sciences : JPS, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 21 citations in OpenAlex.
- Scissor-CIBERSORTx Deconvolution Reveals Functional Heterogeneity of CTAL/aTAL Cells and Associated Biomarkers in Renal Fibrosis.Current issues in molecular biology · 2026Article
- Dual Time-Dependent Effects of Interleukin-33 Administration on the Kidney Postmyocardial Infarction.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2024Article
- Loss of SAV1 in Kidney Proximal Tubule Induces Maladaptive Repair after Ischemia and Reperfusion Injury.International journal of molecular sciences · 2024Article
- 2-Mercaptoethanol protects against DNA double-strand breaks after kidney ischemia and reperfusion injury through GPX4 upregulation.Pharmacological reports : PR · 2022Article
- Molecular Mechanisms of Parthanatos and Its Role in Diverse Diseases.International journal of molecular sciences · 2022Review
- Biomarkers in Primary Focal Segmental Glomerulosclerosis in Optimal Diagnostic-Therapeutic Strategy.Journal of clinical medicine · 2022Review
- Avoid the trap: Targeting PARP1 beyond human malignancy.Cell chemical biology · 2021Review
- Cyclosporin A aggravates hydrogen peroxide-induced cell death in kidney proximal tubule epithelial cells.Anatomy & cell biology · 2019Article
- Exogenous spermidine ameliorates tubular necrosis during cisplatin nephrotoxicity.Anatomy & cell biology · 2018Article
- Spermidine is protective against kidney ischemia and reperfusion injury through inhibiting DNA nitration and PARP1 activation.Anatomy & cell biology · 2017Article
- Poly(ADP-ribose) polymerase 1 contributes to oxidative stress through downregulation of sirtuin 3 during cisplatin nephrotoxicity.Anatomy & cell biology · 2016Article
- Poly(ADP-ribose) polymerase regulates glycolytic activity in kidney proximal tubule epithelial cells.Anatomy & cell biology · 2016Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inactivation of poly(ADP-ribose) polymerase 1 (PARP1) has been found to be protective in several disease models; however, the role of PARP1 in acute kidney injury-induced interstitial fibrosis has not been studied. Herein, we tested whether PARP1 inactivation by treatment with PJ34 (a PARP1 inactivator; 10 mg/kg body weight/day, intraperitoneal implantation of a miniosmotic pump at 2 days after the onset) contributed to the decrease in interstitial fibrosis induced by ischemia-reperfusion injury (IRI) in mouse kidneys. IRI increased PARP1 activation represented by poly(ADP-ribose) expression from 4 to 16 days postinjury, whereas treatment with PJ34 at 2 days after the onset efficaciously abolished the increase in PARP1 activation at 4, 8 and 16 days after IRI. Pharmacological inactivation of PARP1 significantly reduced interstitial fibrosis as represented by the collagen deposition and transforming growth factor-β1 level at 8 and 16 days after IRI. Consistent with collagen deposition, myofibroblast activation represented by α-smooth muscle actin expression was also reduced by PARP1 inactivation at 8 and 16 days after IRI. Furthermore, IRI enhanced macrophage influx, but PARP1 inactivaton remarkably reduced macrophage influx for 4 through 16 days after the injury. Among the chemoattractants for monocytes/macrophages and neutrophils, monocyte chemotactic protein-1 (MCP-1) production in IRI kidneys was significantly reduced by PARP1 inactivation from 4 to 16 days postinjury. These data demonstrate that PARP1 activation contributes to IRI-induced MCP-1 production and in turn to macrophage influx, resulting in the promotion of interstitial fibrosis.
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