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NOX1 triggers ferroptosis and ferritinophagy, contributes to Parkinson's disease
Free Radical Biology and Medicine ( IF 7.1 ) Pub Date : 2024-06-13 , DOI: 10.1016/j.freeradbiomed.2024.06.007 Huiqing Wang 1 , Wenwei Mao 2 , Yuhan Zhang 2 , Wenhui Feng 2 , Bo Bai 2 , Bingyuan Ji 3 , Jing Chen 4 , Baohua Cheng 5 , Fuling Yan 6
Free Radical Biology and Medicine ( IF 7.1 ) Pub Date : 2024-06-13 , DOI: 10.1016/j.freeradbiomed.2024.06.007 Huiqing Wang 1 , Wenwei Mao 2 , Yuhan Zhang 2 , Wenhui Feng 2 , Bo Bai 2 , Bingyuan Ji 3 , Jing Chen 4 , Baohua Cheng 5 , Fuling Yan 6
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The progressive loss of dopaminergic neurons in the midbrain is the hallmark of Parkinson's disease (PD). A newly emerging form of lytic cell death, ferroptosis, has been implicated in PD. However, it remains unclear in terms of PD-associated ferroptosis underlying causative genes and effective therapeutic approaches. This research explored the underlying mechanism of ferroptosis-related genes in PD. Here, Firstly, we found NOX1 associated with ferroptosis differently in PD patients by bioinformatics analysis. and models of PD were constructed to explore the underlying mechanism. PCR, Western blot analysis, immunohistochemistry, immunofluorescence, Ferro orange, and BODIPY C11 were utilized to analyze the levels of ferroptosis. Transcriptomics sequencing was to investigate the downstream pathway and the analysis of immunoprecipitation to validate the upstream factor. In conclusion, NOX1 upregulation and activation of ferroptosis-related neurodegeneration, therefore, might be useful as a clinical therapeutic agent.
中文翻译：
NOX1 引发铁死亡和铁蛋白自噬，导致帕金森病
中脑多巴胺能神经元的逐渐丧失是帕金森病 (PD) 的标志。一种新出现的溶解细胞死亡形式——铁死亡，与帕金森病有关。然而，PD相关铁死亡的致病基因和有效的治疗方法仍不清楚。本研究探讨了PD中铁死亡相关基因的潜在机制。在这里，首先，我们通过生物信息学分析发现NOX1与PD患者的铁死亡有不同的相关性。并构建PD模型以探讨其潜在机制。 PCR、Western blot分析、免疫组织化学、免疫荧光、铁橙和BODIPY C11用于分析铁死亡水平。转录组测序是为了研究下游通路，通过免疫沉淀分析来验证上游因素。总之，NOX1 上调和铁死亡相关神经变性的激活可能可用作临床治疗剂。
更新日期：2024-06-13
中文翻译：
NOX1 引发铁死亡和铁蛋白自噬，导致帕金森病
中脑多巴胺能神经元的逐渐丧失是帕金森病 (PD) 的标志。一种新出现的溶解细胞死亡形式——铁死亡，与帕金森病有关。然而，PD相关铁死亡的致病基因和有效的治疗方法仍不清楚。本研究探讨了PD中铁死亡相关基因的潜在机制。在这里，首先，我们通过生物信息学分析发现NOX1与PD患者的铁死亡有不同的相关性。并构建PD模型以探讨其潜在机制。 PCR、Western blot分析、免疫组织化学、免疫荧光、铁橙和BODIPY C11用于分析铁死亡水平。转录组测序是为了研究下游通路，通过免疫沉淀分析来验证上游因素。总之，NOX1 上调和铁死亡相关神经变性的激活可能可用作临床治疗剂。
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