Royal College of Surgeons in Ireland
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IKK1 aggravates ischemia-reperfusion kidney injury by promoting the differentiation of effector T cells

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journal contribution
posted on 2023-05-08, 13:40 authored by Ning Song, Yang Xu, Hans-Joachim Paust, Ulf Panzer, Maria Mercedes de las Noriega, Linlin Guo, Thomas Renné, Jiabin Huang, Xianglin Meng, Mingyan Zhao, Friedrich Thaiss

Ischemia-reperfusion injury (IRI) is one of the major causes of acute kidney injury (AKI), and experimental work has revealed detailed insight into the inflammatory response in the kidney. T cells and NFκB pathway play an important role in IRI. Therefore, we examined the regulatory role and mechanisms of IkappaB kinase 1 (IKK1) in CD4+T lymphocytes in an experimental model of IRI. IRI was induced in CD4cre and CD4IKK1Δ mice. Compared to control mice, conditional deficiency of IKK1 in CD4+T lymphocyte significantly decreased serum creatinine, blood urea nitrogen (BUN) level, and renal tubular injury score. Mechanistically, lack in IKK1 in CD4+T lymphocytes reduced the ability of CD4 lymphocytes to differentiate into Th1/Th17 cells. Similar to IKK1 gene ablation, pharmacological inhibition of IKK also protected mice from IRI. Together, lymphocyte IKK1 plays a pivotal role in IRI by promoting T cells differentiation into Th1/Th17 and targeting lymphocyte IKK1 may be a novel therapeutic strategy for IRI. 


Open Access funding enabled and organized by Projekt DEAL.

DFG TH 343/12-1

National Natural Scientific Foundation of China 82172164

Heilongjiang Province Key R&D program JD22C005.

China Scholarship Council


Data Availability Statement

All raw data are available via the Sequence Read Archive via GEO (GSE217696).


The original article is available at

Published Citation

Song N, et al. IKK1 aggravates ischemia-reperfusion kidney injury by promoting the differentiation of effector T cells. Cell Mol Life Sci. 2023;80(5):125.

Publication Date

19 April 2023

PubMed ID



  • Irish Centre for Vascular Biology
  • School of Pharmacy and Biomolecular Sciences


Springer Nature


  • Published Version (Version of Record)

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