Scholarlink

<p>Hepatic ischemia-reperfusion injury (IRI) remains an unavoidable consequence of partial hepatic resection and liver transplantation. Oxidative stress damages cellular lipid membranes, causing the formation of oxidized phospholipids (OxPLs), which are members of damage-associated molecular patterns (DAMPs). Nevertheless, the precise mechanism and significance of OxPLs in hepatic IRI are yet to be investigated. Our findings reveal that OxPLs accumulate excessively in the liver after IR. Compared to the control group, pre-treatment with E06 (an OxPLs-neutralizing antibody) significantly alleviates inflammatory cell infiltration and liver injury following IR. In vitro experiments show that OxPLs inhibit macrophage autophagy, thereby promoting M1 polarization. This regulatory effect depends on the activation of the Wnt/β-Catenin pathway by OxPLs.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Oxidized Phospholipids Aggravate Hepatic Ischemia/Reperfusion Injury by Promoting Macrophage M1 Polarization Via Regulating the Wnt/β-catenin/Autophagy Axis

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年2月6日

查看全文
  • Minhao Chen,
  • Yue Liu,
  • Jie Li,
  • Ziyi Wang,
  • Yu Zhang,
  • Xuejiao Chen,
  • Xiangdong Li,
  • Nan Xia,
  • Wenjie Yu,
  • Linfeng Sun,
  • Yuhao Xiao,
  • Haoliang Zhu,
  • Jie Wei,
  • Liyong Pu,
  • Sheng Han

摘要

Hepatic ischemia-reperfusion injury (IRI) remains an unavoidable consequence of partial hepatic resection and liver transplantation. Oxidative stress damages cellular lipid membranes, causing the formation of oxidized phospholipids (OxPLs), which are members of damage-associated molecular patterns (DAMPs). Nevertheless, the precise mechanism and significance of OxPLs in hepatic IRI are yet to be investigated. Our findings reveal that OxPLs accumulate excessively in the liver after IR. Compared to the control group, pre-treatment with E06 (an OxPLs-neutralizing antibody) significantly alleviates inflammatory cell infiltration and liver injury following IR. In vitro experiments show that OxPLs inhibit macrophage autophagy, thereby promoting M1 polarization. This regulatory effect depends on the activation of the Wnt/β-Catenin pathway by OxPLs.