Liproxstatin-1 Alleviated Ischemia/Reperfusion-Induced Acute Kidney Injury via Inhibiting Ferroptosis
Ferroptosis, as a novel regulable cell death, is characterized by iron overload, glutathione depletion, and an accumulation of lipid peroxides. Recently, it has been discovered that ferroptosis is involved in ischemia/reperfusion (I/R)-induced acute kidney injury (AKI) and plays a crucial role in renal tubular cell death. In this study, we tried to investigate the effect and mechanism of liproxstatin-1 (Lip-1) in I/R-induced AKI and seek the key regulator of ferroptosis in I/R-induced AKI. Mice were administrated with clamping bilateral renal pedicles for 30 min. We found that early growth response 1 (EGR1) might be a key regulator of ferroptosis, and Lip-1 could suppress ferroptosis via EGR1. Meanwhile, Lip-1 could reduce macrophage recruitment and the release of inflammatory cytokines. These findings indicated that Lip-1 alleviated I/R-induced AKI via regulating EGR1, and it might pave the theoretical basis of a new therapeutic strategy for I/R-induced AKI.
Medienart: |
E-Artikel |
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Erscheinungsjahr: |
2024 |
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Erschienen: |
2024 |
Enthalten in: |
Zur Gesamtaufnahme - volume:13 |
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Enthalten in: |
Antioxidants (Basel, Switzerland) - 13(2024), 2 vom: 31. Jan. |
Sprache: |
Englisch |
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Beteiligte Personen: |
Shi, Zhiyuan [VerfasserIn] |
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Links: |
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Themen: |
Acute kidney injury |
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Anmerkungen: |
Date Revised 27.02.2024 published: Electronic Citation Status PubMed-not-MEDLINE |
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doi: |
10.3390/antiox13020182 |
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funding: |
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Förderinstitution / Projekttitel: |
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PPN (Katalog-ID): |
NLM368877590 |
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520 | |a Ferroptosis, as a novel regulable cell death, is characterized by iron overload, glutathione depletion, and an accumulation of lipid peroxides. Recently, it has been discovered that ferroptosis is involved in ischemia/reperfusion (I/R)-induced acute kidney injury (AKI) and plays a crucial role in renal tubular cell death. In this study, we tried to investigate the effect and mechanism of liproxstatin-1 (Lip-1) in I/R-induced AKI and seek the key regulator of ferroptosis in I/R-induced AKI. Mice were administrated with clamping bilateral renal pedicles for 30 min. We found that early growth response 1 (EGR1) might be a key regulator of ferroptosis, and Lip-1 could suppress ferroptosis via EGR1. Meanwhile, Lip-1 could reduce macrophage recruitment and the release of inflammatory cytokines. These findings indicated that Lip-1 alleviated I/R-induced AKI via regulating EGR1, and it might pave the theoretical basis of a new therapeutic strategy for I/R-induced AKI | ||
650 | 4 | |a Journal Article | |
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700 | 1 | |a Tang, Wenbin |e verfasserin |4 aut | |
700 | 1 | |a Liang, Qing |e verfasserin |4 aut | |
700 | 1 | |a Zheng, Zeyuan |e verfasserin |4 aut | |
700 | 1 | |a Liu, Bin |e verfasserin |4 aut | |
700 | 1 | |a Sun, Huimin |e verfasserin |4 aut | |
700 | 1 | |a Wang, Kejia |e verfasserin |4 aut | |
700 | 1 | |a Shao, Chen |e verfasserin |4 aut | |
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