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IKK1 aggravates ischemia-reperfusion kidney injury by promoting the differentiation of effector T cells

Standard

IKK1 aggravates ischemia-reperfusion kidney injury by promoting the differentiation of effector T cells. / Song, Ning; Xu, Yang; Paust, Hans-Joachim; Panzer, Ulf; Noriega, Maria de las Mercedes; Guo, Linlin; Renne, Thomas; Huang, Jiabin; Meng, Xianglin; Zhao, Mingyan; Thaiss, Friedrich.

in: CELL MOL LIFE SCI, Jahrgang 80, Nr. 5, 19.04.2023, S. 125.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Song, N, Xu, Y, Paust, H-J, Panzer, U, Noriega, MDLM, Guo, L, Renne, T, Huang, J, Meng, X, Zhao, M & Thaiss, F 2023, 'IKK1 aggravates ischemia-reperfusion kidney injury by promoting the differentiation of effector T cells', CELL MOL LIFE SCI, Jg. 80, Nr. 5, S. 125. https://doi.org/10.1007/s00018-023-04763-2

APA

Song, N., Xu, Y., Paust, H-J., Panzer, U., Noriega, M. D. L. M., Guo, L., Renne, T., Huang, J., Meng, X., Zhao, M., & Thaiss, F. (2023). IKK1 aggravates ischemia-reperfusion kidney injury by promoting the differentiation of effector T cells. CELL MOL LIFE SCI, 80(5), 125. https://doi.org/10.1007/s00018-023-04763-2

Vancouver

Song N, Xu Y, Paust H-J, Panzer U, Noriega MDLM, Guo L et al. IKK1 aggravates ischemia-reperfusion kidney injury by promoting the differentiation of effector T cells. CELL MOL LIFE SCI. 2023 Apr 19;80(5):125. https://doi.org/10.1007/s00018-023-04763-2

Bibtex

@article{f0ca6606b53d491bbb57f5046e292fc4,
title = "IKK1 aggravates ischemia-reperfusion kidney injury by promoting the differentiation of effector T cells",
abstract = "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.",
author = "Ning Song and Yang Xu and Hans-Joachim Paust and Ulf Panzer and Noriega, {Maria de las Mercedes} and Linlin Guo and Thomas Renne and Jiabin Huang and Xianglin Meng and Mingyan Zhao and Friedrich Thaiss",
year = "2023",
month = apr,
day = "19",
doi = "10.1007/s00018-023-04763-2",
language = "English",
volume = "80",
pages = "125",
journal = "CELL MOL LIFE SCI",
issn = "1420-682X",
publisher = "Birkhauser Verlag Basel",
number = "5",

}

RIS

TY - JOUR

T1 - IKK1 aggravates ischemia-reperfusion kidney injury by promoting the differentiation of effector T cells

AU - Song, Ning

AU - Xu, Yang

AU - Paust, Hans-Joachim

AU - Panzer, Ulf

AU - Noriega, Maria de las Mercedes

AU - Guo, Linlin

AU - Renne, Thomas

AU - Huang, Jiabin

AU - Meng, Xianglin

AU - Zhao, Mingyan

AU - Thaiss, Friedrich

PY - 2023/4/19

Y1 - 2023/4/19

N2 - 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.

AB - 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.

U2 - 10.1007/s00018-023-04763-2

DO - 10.1007/s00018-023-04763-2

M3 - SCORING: Journal article

C2 - 37074502

VL - 80

SP - 125

JO - CELL MOL LIFE SCI

JF - CELL MOL LIFE SCI

SN - 1420-682X

IS - 5

ER -