Mitochondria are the power plants of the cell, their proper function is crucial for cellular function and homeostasis. Mitophagy regulates mitochondrial content/quality by selectively removing damaged mitochondria. Zinc is one of the most essential trace elements in the body. The concentration of intracellular free zinc is strictly regulated maintained, known as zinc homeostasis. Zinc homeostasis is achieved by proteins and organelles which sequester zinc. The abnormal zinc concentration has been implicated in numerous clinical manifestations including ischemic stroke. Emerging evidence over the past decade has shown that that zinc affects mitochondria in response to ischemia. It is progressively clear that zinc‐mitochondrial interactions occur in and contribute to ischemic injury. Among the pathological effects of zinc accumulation on mitochondria, zinc induced release and accumulation of ROS draws special interest. ROS is a major cause of mitochondrial damage and initiates mitophagy. In addition, emerging evidence suggests that mitophagy plays critical roles in the pathophysiological process of cerebral ischemia. In the present study I analyzed the role of zinc and mitophagy in hypoxia‐induced mitophagy and investigated the signaling pathways between zinc and mitophagy under hypoxia condition.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.