HIF-1α/BNIP3通过自噬介导的内质网降解可防止缺血再灌注引起的急性肾损伤。

IF 5.9 2区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY
Hao Zhao, Ming Yang, Yachun Han, Na Jiang, Yan Liu, Chenrui Li, Jinfei Yang, Shilu Luo, Chongbin Liu, Lin Sun, Fuyou Liu, Yu Liu
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引用次数: 0

摘要

内质网(ER)通过自噬降解是细胞处于应激状态时维持ER平衡的一个过程,与许多疾病相关;然而,缺氧诱导因子-1α(HIF-1α)介导的ER降解及其相关调控途径在急性肾损伤(AKI)中的作用仍有待进一步确定。本研究通过缺血再灌注(IR)法诱导小鼠建立了体内 AKI 模型。结果发现,AKI小鼠肾脏中HIF-1α和BNIP3增高,自噬和ER降解被激活,而HIF-1α敲除能显著抑制BNIP3、自噬和ER降解,并伴随肾损伤加重。体外过表达 HIF-1α 能明显增加 BNIP3、自噬和 ER 降解,而抑制 BNIP3 则能明显逆转 HIF-1α 的影响。此外,用氯喹体外抑制自噬也能明显逆转 HIF-1α 对细胞凋亡的影响。此外,在体外选择性地在 ER 膜上过表达 BNIP3 能显著增加 ER 通过自噬的降解,减少细胞凋亡。这些数据表明,在肾小管细胞中,HIF-1α/BNIP3 通过自噬介导的ER降解对红外诱导的 AKI 有保护作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
HIF-1α/BNIP3-Mediated Endoplasmic Reticulum Degradation via Autophagy Protects Against Ischemia Reperfusion-Induced Acute Kidney Injury.
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来源期刊
Antioxidants & redox signaling
Antioxidants & redox signaling 生物-内分泌学与代谢
CiteScore
14.10
自引率
1.50%
发文量
170
审稿时长
3-6 weeks
期刊介绍: Antioxidants & Redox Signaling (ARS) is the leading peer-reviewed journal dedicated to understanding the vital impact of oxygen and oxidation-reduction (redox) processes on human health and disease. The Journal explores key issues in genetic, pharmaceutical, and nutritional redox-based therapeutics. Cutting-edge research focuses on structural biology, stem cells, regenerative medicine, epigenetics, imaging, clinical outcomes, and preventive and therapeutic nutrition, among other areas. ARS has expanded to create two unique foci within one journal: ARS Discoveries and ARS Therapeutics. ARS Discoveries (24 issues) publishes the highest-caliber breakthroughs in basic and applied research. ARS Therapeutics (12 issues) is the first publication of its kind that will help enhance the entire field of redox biology by showcasing the potential of redox sciences to change health outcomes. ARS coverage includes: -ROS/RNS as messengers -Gaseous signal transducers -Hypoxia and tissue oxygenation -microRNA -Prokaryotic systems -Lessons from plant biology
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