ArticleAntioxidants (Basel, Switzerland)2021
CCN2 Aggravates the Immediate Oxidative Stress-DNA Damage Response following Renal Ischemia-Reperfusion Injury.
Article in Antioxidants (Basel, Switzerland), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 32 citations in OpenAlex.
- N-acetyl cysteine amide mitigates oxidative stress and apoptosis in a rat model of renal ischemia-reperfusion injury.Scientific reports · 2026Article
- Dasatinib and Quercetin Combination Increased Kidney Damage in Acute Folic Acid-Induced Experimental Nephropathy.Pharmaceuticals (Basel, Switzerland) · 2025Article
- CCN2 Activates Cellular Senescence Leading to Kidney Fibrosis in Folic Acid-Induced Experimental Nephropathy.International journal of molecular sciences · 2025Article
- Update of cellular senescence in kidney fibrosis: from mechanism to potential interventions.Frontiers of medicine · 2025Review
- Protective effects of pioglitazone in renal ischemia-reperfusion injury (RIRI): focus on oxidative stress and inflammation.Clinical and experimental nephrology · 2024Review
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- The potential renoprotective effect of Raloxifene in renal ischemia-reperfusion injury in a male rat model.Journal of medicine and life · 2023Article
- CCN2 Activates RIPK3, NLRP3 Inflammasome, and NRF2/Oxidative Pathways Linked to Kidney Inflammation.Antioxidants (Basel, Switzerland) · 2023Article
- CCN proteins: opportunities for clinical studies-a personal perspective.Journal of cell communication and signaling · 2023Review
- HMOX1 silencing prevents doxorubicin-induced cardiomyocyte injury, mitochondrial dysfunction, and ferroptosis by downregulating CTGF.General thoracic and cardiovascular surgery · 2023Article
- Vitamin D, Cellular Senescence and Chronic Kidney Diseases: What Is Missing in the Equation?Nutrients · 2023Review
- Myrrh Essential Oil Mitigates Renal Ischemia/Reperfusion-Induced Injury.Current issues in molecular biology · 2023Article
- Cellular senescence of renal tubular epithelial cells in renal fibrosis.Frontiers in endocrinology · 2023Review
- Roles of DNA damage in renal tubular epithelial cells injury.Frontiers in physiology · 2023Review
- Regulated necrosis role in inflammation and repair in acute kidney injury.Frontiers in immunology · 2023Review
- CCN2 Binds to Tubular Epithelial Cells in the Kidney.Biomolecules · 2022Article
- Inhibition of PLK3 Attenuates Tubular Epithelial Cell Apoptosis after Renal Ischemia-Reperfusion Injury by Blocking the ATM/P53-Mediated DNA Damage Response.Oxidative medicine and cellular longevity · 2022Article
- MicroRNA-34a: A Novel Therapeutic Target in Fibrosis.Frontiers in physiology · 2022Review
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
AKI, due to the fact of altered oxygen supply after kidney transplantation, is characterized by renal ischemia-reperfusion injury (IRI). Recent data suggest that AKI to CKD progression may be driven by cellular senescence evolving from prolonged DNA damage response (DDR) following oxidative stress. Cellular communication factor 2 (CCN2, formerly called CTGF) is a major contributor to CKD development and was found to aggravate DNA damage and the subsequent DDR-cellular senescence-fibrosis sequence following renal IRI. We therefore investigated the impact of CCN2 inhibition on oxidative stress and DDR in vivo and in vitro. Four hours after reperfusion, full transcriptome RNA sequencing of mouse IRI kidneys revealed CCN2-dependent enrichment of several signaling pathways, reflecting a different immediate stress response to IRI. Furthermore, decreased staining for γH2AX and p-p53 indicated reduced DNA damage and DDR in tubular epithelial cells of CCN2 knockout (KO) mice. Three days after IRI, DNA damage and DDR were still reduced in CCN2 KO, and this was associated with reduced oxidative stress, marked by lower lipid peroxidation, protein nitrosylation, and kidney expression levels of Nrf2 target genes (i.e., HMOX1 and NQO1). Finally, silencing of CCN2 alleviated DDR and lipid peroxidation induced by anoxia-reoxygenation injury in cultured PTECs. Together, our observations suggest that CCN2 inhibition might mitigate AKI by reducing oxidative stress-induced DNA damage and the subsequent DDR. Thus, targeting CCN2 might help to limit post-IRI AKI.
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