Duan Wenqi, Wu Wenye, Yang Cui, Zhang Mei, Li Xuemei, Tian Wenmin, Chen Yang, Zhang Xinjun
Key Laboratory of Molecular Biophysics of the Ministry of Education, College of Life Science and Technology, Huazhong University of Science and Technology, Wuhan, China.
Research Unit for Blindness Prevention of the Chinese Academy of Medical Sciences (2019RU026), Sichuan Academy of Medical Sciences and Sichuan Provincial People's Hospital, Chengdu, China.
Front Cell Dev Biol. 2025 Jul 24;13:1619339. doi: 10.3389/fcell.2025.1619339. eCollection 2025.
Mitochondria serve as hubs for many critical cellular processes, and their functions and dynamics are tightly controlled. TRABD is a Tiki/TraB family protein with unknown function. Here, we characterized TRABD as a novel outer mitochondrial membrane protein. Depletion of in cells severely impairs mitochondrial respiration and ATP production, inhibits cell growth, increases reactive oxygen species levels. Depletion of also affects mitochondrial dynamics and mitophagy, possibly through interactions with PGAM5. Knockout of in mice significantly exacerbates ischemia reperfusion-induced renal tubular injury by promoting mitochondrial fragmentation and damage. Our study identified a novel outer mitochondrial membrane protein and revealed the critical roles of TRABD in mitochondrial dynamics and ischemia reperfusion-induced renal tubular injury.
线粒体是许多关键细胞过程的枢纽，其功能和动态受到严格控制。TRABD是一种功能未知的Tiki/TraB家族蛋白。在这里，我们将TRABD鉴定为一种新型线粒体外膜蛋白。细胞中TRABD的缺失严重损害线粒体呼吸和ATP产生，抑制细胞生长，增加活性氧水平。TRABD的缺失还可能通过与PGAM5相互作用影响线粒体动态和线粒体自噬。小鼠中TRABD的敲除通过促进线粒体碎片化和损伤显著加剧缺血再灌注诱导的肾小管损伤。我们的研究鉴定了一种新型线粒体外膜蛋白，并揭示了TRABD在线粒体动态和缺血再灌注诱导的肾小管损伤中的关键作用。
