帕金
粒体自噬
品脱1
炎症体
线粒体
肾毒性
神经毒性
细胞生物学
化学
药理学
生物
细胞凋亡
肾
免疫学
医学
自噬
生物化学
内分泌学
炎症
内科学
毒性
帕金森病
有机化学
疾病
作者
Xuliang Zhang,Jiayu Du,Bo Li,Siming Huo,Jian Zhang,Yilong Cui,Miao Song,Bing Shao,Yanfei Li
标识
DOI:10.1016/j.fct.2022.113078
摘要
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.
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