Renalase as a Novel Biomarker for Evaluating the Severity of Hepatic Ischemia-Reperfusion Injury

Li, Huili; Guo, Jianxin; Liu, Hongli; Niu, Yanfeng; Wang, Lixia; Huang, Kun; Wang, Jiliang

doi:10.1155/2016/3178562

Cited by 13 publications

(18 citation statements)

References 53 publications

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“…Our study also confirmed that OA was able to limit intracellular lipid peroxidation levels induced by H 2 O 2 . Our previous study found that renalase is highly sensitive and responsive to oxidative stress in vitro and in vivo [35]. In this study, we found OA decreased the expression of renalase induced by H 2 O 2 .…”

Section: Discussionsupporting

confidence: 55%

Oleic Acid Protects against Hepatic Ischemia and Reperfusion Injury in Mice by Inhibiting AKT/mTOR Pathways

Guo

Zhang

et al. 2019

Oxidative Medicine and Cellular Longevity

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Hepatic ischemia-reperfusion (I/R) injury is a serious complication in patients who have undergone hepatic surgery such as orthotopic liver transplantation and partial hepatectomy. Recently, a new cytoprotective agent, ursodeoxycholyl lysophosphatidylethanolamide (UDCA-LPE), was reported to protect against hepatic I/R injury. However, the protective mechanism of UDCA-LPE is not fully understood. Therefore, we conducted this study to explore its underlying mechanism. We used liquid chromatography-tandem mass spectrometry (LC-MS/MS) to analyze the liver lipid metabolism changes in mice during I/R. KEGG enrichment indicated that UDCA-LPE is likely to exert its protective role by regulating fatty acid (FA) metabolism. Further analysis found that UDCA-LPE significantly increased the ratio of oleic acid (OA) to palmitic acid (PA). We found that mice pretreated with OA improved tolerance to hepatic I/R injury. In addition, the phosphorylation level of AKT was markedly upregulated during oxidative stress to promote p65 nuclear translocation, triggering an inflammatory response that exacerbated cell damage and OA treatment significantly inhibited this process. Notably, OA was found to inhibit H2O2-induced oxidative stress, inflammation, and cell death in HepG2 cells. Furthermore, we found that OA supplementation to the medium did not result in a significant increase in intracellular OA, but marked increase in the ratio of OA to PA, which may be an important mechanism for the inflammatory response induced by oxidative stress during I/R. Finally, we demonstrated that OA increased the level of autophagy in HepG2 cells, which may be one of the protective mechanisms against oxidative stress. Collectively, this study revealed that FA metabolism functionally determines the oxidative stress-related inflammation caused by hepatic I/R. We hypothesize that OA treatment may be a promising strategy for preventing and treating I/R-induced liver damage.

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Section: Discussionsupporting

confidence: 55%

Oleic Acid Protects against Hepatic Ischemia and Reperfusion Injury in Mice by Inhibiting AKT/mTOR Pathways

Guo

Zhang

et al. 2019

Oxidative Medicine and Cellular Longevity

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“…Although the antioxidant effect could not be measured in this study, it could be a possible cause of the decrease of TBARS 22,23) . The study of Li et al showed a significant increase in renalase expression with increasing oxidative stress in a mice model of ischemia-reperfusion injury, and it was suppressed by antioxidants 24) . In addition, it has been reported that renalase increases during ischemiareperfusion and has the effect of protecting organs [25][26][27] .…”

Section: Discussionmentioning

confidence: 98%

Transient changes in serum renalase concentration during long-distance running: The case of an amateur runner under continuous training

Yoshida

Sugasawa

Hoshino

et al. 2017

JPFSM

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“…Wu et al showed that TGF-β increases the levels of fibrosis markers such as α-smooth muscle actin (α-SMA), E-cadherin, and collagen type I α 1 (Col1a1) in human kidney 2 cells (15). In addition, hepatic renalase expression increases in response to oxidative stress in the mouse liver with induced ischemia-reperfusion (IR) injury, suggesting that renalase protects tissues (16). Recently, the downregulation of renalase in nonalcoholic fatty liver disease (NAFLD) and its protective role against liver IR injury has been reported, indicating that the downregulation of renalase may be involved in the susceptibility of the fatty liver to IR injury (17).…”

Section: Effects Of Renalase Deficiency On Liver Fibrosis Markers Inmentioning

confidence: 99%

Effects of renalase deficiency on liver fibrosis markers in a nonalcoholic steatohepatitis mouse model

et al. 2021

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Progression of nonalcoholic steatohepatitis (NASH) is attributed to several factors, including inflammation and oxidative stress. In recent years, renalase has been reported to suppress oxidative stress, apoptosis and inflammation. A number of studies have suggested that renalase may be associated with protecting the liver from injury. The present study aimed to clarify the effects of renalase knockout (KO) in mice with NASH that were induced with a choline-deficient high-fat diet (CDAHFD) supplemented with 0.1% methionine. Wild type (WT) and KO mice (6-week-old) were fed a normal diet (ND) or CDAHFD for 6 weeks, followed by analysis of the blood liver function markers and liver tissues. CDAHFD intake was revealed to increase blood hepatic function markers, lipid accumulation and oxidative stress compared with ND, but no significant differences were observed between the WT and KO mice. However, in the KO-CDAHFD group, the Adgre1 and Tgfb1 mRNA levels were significantly higher, and α-SMA expression was significantly lower compared with the WT-CDAHFD group. Furthermore, the Gclc mRNA and phosphorylated protein kinase B (Akt) levels were significantly lower in the KO-ND group compared with the WT-ND group. The results of the current study indicated that as NASH progressed in the absence of renalase, oxidative stress, macrophage infiltration and TGF-β expression were enhanced, while α-SMA expression in NASH may be partly suppressed due to the decreased phosphorylation of Akt level.

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Renalase as a Novel Biomarker for Evaluating the Severity of Hepatic Ischemia-Reperfusion Injury

Cited by 13 publications

References 53 publications

Oleic Acid Protects against Hepatic Ischemia and Reperfusion Injury in Mice by Inhibiting AKT/mTOR Pathways

Oleic Acid Protects against Hepatic Ischemia and Reperfusion Injury in Mice by Inhibiting AKT/mTOR Pathways

Transient changes in serum renalase concentration during long-distance running: The case of an amateur runner under continuous training

Effects of renalase deficiency on liver fibrosis markers in a nonalcoholic steatohepatitis mouse model

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