TRABD maintains mitochondrial homeostasis and protects against ischemia reperfusion-induced renal tubular injury

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 <i>TRABD</i> in cells severely impairs mitochondrial respiration and ATP production, inhibits cell growth, increases reactive oxygen species levels. Depletion of <i>TRABD</i> also affects mitochondrial dynamics and mitophagy, possibly through interactions with PGAM5. Knockout of <i>TRABD</i> 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.