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20240411232422.0 |
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240308s2024 xx |||||o 00| ||eng c |
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|a 10.1016/j.clim.2024.110167
|2 doi
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|a pubmed24n1372.xml
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|a (DE-627)NLM369428773
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|a (NLM)38453127
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|a (PII)S1521-6616(24)00058-5
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|a DE-627
|b ger
|c DE-627
|e rakwb
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| 041 |
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|a eng
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| 100 |
1 |
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|a Tie, Hongtao
|e verfasserin
|4 aut
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| 245 |
1 |
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|a LXA4 protected mice from renal ischemia/reperfusion injury by promoting IRG1/Nrf2 and IRAK-M-TRAF6 signal pathways
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|c 2024
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|a Text
|b txt
|2 rdacontent
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|a ƒaComputermedien
|b c
|2 rdamedia
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| 338 |
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|a ƒa Online-Ressource
|b cr
|2 rdacarrier
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| 500 |
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|a Date Completed 18.03.2024
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|a Date Revised 10.04.2024
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|a published: Print-Electronic
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|a Citation Status MEDLINE
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|a Copyright © 2024 Elsevier Inc. All rights reserved.
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|a Excessive inflammatory response and increased oxidative stress play an essential role in the pathophysiology of ischemia/reperfusion (I/R)-induced acute kidney injury (IRI-AKI). Emerging evidence suggests that lipoxin A4 (LXA4), as an endogenous negative regulator in inflammation, can ameliorate several I/R injuries. However, the mechanisms and effects of LXA4 on IRI-AKI remain unknown. In this study, A bilateral renal I/R mouse model was used to evaluate the role of LXA4 in wild-type, IRG1 knockout, and IRAK-M knockout mice. Our results showed that LXA4, as well as 5-LOX and ALXR, were quickly induced, and subsequently decreased by renal I/R. LXA4 pretreatment improved renal I/R-induced renal function impairment and renal damage and inhibited inflammatory responses and oxidative stresses in mice kidneys. Notably, LXA4 inhibited I/R-induced the activation of TLR4 signal pathway including decreased phosphorylation of TAK1, p36, and p65, but did not affect TLR4 and p-IRAK-1. The analysis of transcriptomic sequencing data and immunoblotting suggested that innate immune signal molecules interleukin-1 receptor-associated kinase-M (IRAK-M) and immunoresponsive gene 1 (IRG1) might be the key targets of LXA4. Further, the knockout of IRG1 or IRAK-M abolished the beneficial effects of LXA4 on IRI-AKI. In addition, IRG1 deficiency reversed the up-regulation of IRAK-M by LXA4, while IRAK-M knockout had no impact on the IRG1 expression, indicating that IRAK-M is a downstream molecule of IRG1. Mechanistically, we found that LXA4-promoted IRG1-itaconate not only enhanced Nrf2 activation and increased HO-1 and NQO1, but also upregulated IRAK-M, which interacted with TRAF6 by competing with IRAK-1, resulting in deactivation of TLR4 downstream signal in IRI-AKI. These data suggested that LXA4 protected against IRI-AKI via promoting IRG1/Itaconate-Nrf2 and IRAK-M-TRAF6 signaling pathways, providing the rationale for a novel strategy for preventing and treating IRI-AKI
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|a Journal Article
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|a Research Support, Non-U.S. Gov't
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4 |
|a IRAK-M
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4 |
|a IRG1
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| 650 |
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4 |
|a Ischemia/reperfusion
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| 650 |
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4 |
|a Lipoxin A4
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| 650 |
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4 |
|a Nrf2
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| 650 |
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7 |
|a lipoxin A4
|2 NLM
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| 650 |
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7 |
|a itaconic acid
|2 NLM
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| 650 |
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7 |
|a Q4516562YH
|2 NLM
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| 650 |
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7 |
|a NF-E2-Related Factor 2
|2 NLM
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| 650 |
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7 |
|a TNF Receptor-Associated Factor 6
|2 NLM
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| 650 |
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7 |
|a Toll-Like Receptor 4
|2 NLM
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| 650 |
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7 |
|a Interleukin-1 Receptor-Associated Kinases
|2 NLM
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| 650 |
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7 |
|a EC 2.7.11.1
|2 NLM
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| 650 |
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|a Succinates
|2 NLM
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| 650 |
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7 |
|a Lipoxins
|2 NLM
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| 700 |
1 |
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|a Kuang, Ge
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Gong, Xia
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Zhang, Lidan
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Zhao, Zizuo
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Wu, Shengwang
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Huang, Wenya
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Chen, Xiahong
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Yuan, Yinglin
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Li, Zhenhan
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Li, Hongzhong
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Zhang, Li
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Wan, Jingyuan
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Wang, Bin
|e verfasserin
|4 aut
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| 773 |
0 |
8 |
|i Enthalten in
|t Clinical immunology (Orlando, Fla.)
|d 1999
|g 261(2024) vom: 05. Apr., Seite 110167
|w (DE-627)NLM098196855
|x 1521-7035
|7 nnns
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| 773 |
1 |
8 |
|g volume:261
|g year:2024
|g day:05
|g month:04
|g pages:110167
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| 856 |
4 |
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|u http://dx.doi.org/10.1016/j.clim.2024.110167
|3 Volltext
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|a GBV_ILN_11
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|a GBV_ILN_24
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|a AR
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|d 261
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