ArticleJournal of the American Heart Association2017
Inhibition of IκB Kinase at 24 Hours After Acute Kidney Injury Improves Recovery of Renal Function and Attenuates Fibrosis.
Article in Journal of the American Heart Association, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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Who cites it
24 citing papers in PubMed, 28 citations in OpenAlex.
- Acute renal injury in ANCA-associated glomerulonephritis: etiology related to acute tubulointerstitial injury versus glomerular injury.Renal failure · 2026Article
- Nucleic acid sensing pathways in kidney disease development.Nature reviews. Nephrology · 2026Review
- T-Cell Remodeling in Renal Fibrosis: From Acute Injury to Chronic Kidney Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Monocytes strongly induce (myo)fibroblast contraction in a 3D skin model to understand inflammation-fibrosis crosstalk.Scientific reports · 2026Article
- Tri-domain proteins 27 alleviates ischemia-reperfusion injury-induced acute kidney injury by promoting Gli-like transcription factor 1 expression via the inhibition of polycomb repressive complex 2 activity.Journal of cell communication and signaling · 2025Article
- Article
- Advance in Iron Metabolism, Oxidative Stress and Cellular Dysfunction in Experimental and Human Kidney Diseases.Antioxidants (Basel, Switzerland) · 2024Review
- The role of nitric oxide in sepsis-associated kidney injury.Bioscience reports · 2022Article
- Bruton's TK regulates myeloid cell recruitment during acute inflammation.British journal of pharmacology · 2022Article
- Advancements in nanomedicines for the detection and treatment of diabetic kidney disease.Biomaterials and biosystems · 2022Review
- The interaction between cellular senescence and chronic kidney disease as a therapeutic opportunity.Frontiers in pharmacology · 2022Review
- Advances in Immunosuppressive Agents Based on Signal Pathway.Frontiers in pharmacology · 2022Review
- Recent Approaches to Targeting Canonical NFJournal of the American Society of Nephrology : JASN · 2021Review
- Genetic Susceptibility to Acute Kidney Injury.Journal of clinical medicine · 2021Review
- Ginaton injection alleviates cisplatin-induced renal interstitial fibrosis in rats via inhibition of apoptosis through regulation of the p38MAPK/TGF-β1 and p38MAPK/HIF-1α pathways.Biomedical reports · 2021Article
- Lipidomics Provides New Insight into Pathogenesis and Therapeutic Targets of the Ischemia-Reperfusion Injury.International journal of molecular sciences · 2021Review
- Review
- Silibinin enhances anti-renal fibrosis effect of MK-521 via downregulation of TGF-β signaling pathway.Human cell · 2020Article
- Senescence and the Aging Immune System as Major Drivers of Chronic Kidney Disease.Frontiers in cell and developmental biology · 2020Review
- The MEK Inhibitor Trametinib Ameliorates Kidney Fibrosis by Suppressing ERK1/2 and mTORC1 Signaling.Journal of the American Society of Nephrology : JASN · 2019Article
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAcute kidney injury (AKI) is a major risk factor for the development of chronic kidney disease. Nuclear factor-κB is a nuclear transcription factor activated post-ischemia, responsible for the transcription of proinflammatory proteins. The role of nuclear factor-κB in the renal fibrosis post-AKI is unknown. METHODS AND
resultsWe used a rat model of AKI caused by unilateral nephrectomy plus contralateral ischemia (30 minutes) and reperfusion injury (up to 28 days) to show impairment of renal function (peak: 24 hours), activation of nuclear factor-κB (peak: 48 hours), and fibrosis (28 days). In humans, AKI is diagnosed by a rise in serum creatinine. We have discovered that the IκB kinase inhibitor IKK16 (even when given at peak serum creatinine) still improved functional and structural recovery and reduced myofibroblast formation, macrophage infiltration, transforming growth factor-β expression, and Smad2/3 phosphorylation. AKI resulted in fibrosis within 28 days (Sirius red staining, expression of fibronectin), which was abolished by IKK16. To confirm the efficacy of IKK16 in a more severe model of fibrosis, animals were subject to 14 days of unilateral ureteral obstruction, resulting in tubulointerstitial fibrosis, myofibroblast formation, and macrophage infiltration, all of which were attenuated by IKK16.
conclusionsInhibition of IκB kinase at peak creatinine improves functional recovery, reduces further injury, and prevents fibrosis.
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