PINK1/Parkin 介导的线粒体自噬减轻了 T-2 毒素诱导的肾毒性。
PINK1/Parkin-mediated mitophagy mitigates T-2 toxin-induced nephrotoxicity.
机构信息
Key Laboratory of the Provincial Education, Department of Heilongjiang for Common Animal Disease Prevention and Treatment, College of Veterinary Medicine, Northeast Agricultural University, Harbin, 150030, China.
Key Laboratory of the Provincial Education, Department of Heilongjiang for Common Animal Disease Prevention and Treatment, College of Veterinary Medicine, Northeast Agricultural University, Harbin, 150030, China.
出版信息
Food Chem Toxicol. 2022 Jun;164:113078. doi: 10.1016/j.fct.2022.113078. Epub 2022 Apr 27.
T-2 toxin can cause mitochondrial impairment and subsequent renal damage. PINK1/Parkin-mediated mitophagy can mitigate renal impairment by alleviating mitochondrial damage. Nevertheless, the impact of PINK1/Parkin-mediated mitophagy in T-2 toxin-induced renal injury remains unclear. Here, we studied the role of PINK1/Parkin-mediated mitophagy in T-2 toxin-induced nephrotoxicity. Mitochondrial damage was accompanied by NLRP3-inflammasome activation and PINK1/Parkin-mediated mitophagy in the kidney of T-2 toxin-exposed C57BL/6N mice. Knocking out Parkin inhibited the mitophagy but aggravated the structural and functional damage, NLRP3-inflammasome activation, mitochondrial damage, and apoptosis. Correlation analysis revealed that NLRP3-inflammasome activation was correlated with apoptosis. These results show that PINK1/Parkin-mediated mitophagy mitigates T-2 toxin-induced nephrotoxicity.
T-2 毒素可导致线粒体损伤和随后的肾脏损伤。PINK1/Parkin 介导的线粒体自噬可以通过减轻线粒体损伤来减轻肾脏损伤。然而，PINK1/Parkin 介导的线粒体自噬在 T-2 毒素诱导的肾损伤中的作用尚不清楚。在这里，我们研究了 PINK1/Parkin 介导的线粒体自噬在 T-2 毒素诱导的肾毒性中的作用。在 T-2 毒素暴露的 C57BL/6N 小鼠的肾脏中，线粒体损伤伴随着 NLRP3 炎性小体的激活和 PINK1/Parkin 介导的线粒体自噬。敲除 Parkin 抑制了线粒体自噬，但加重了结构和功能损伤、NLRP3 炎性小体激活、线粒体损伤和细胞凋亡。相关性分析显示，NLRP3 炎性小体激活与细胞凋亡相关。这些结果表明，PINK1/Parkin 介导的线粒体自噬减轻了 T-2 毒素诱导的肾毒性。
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