Mitochondria autophagy, termed as mitophagy, is a mechanism of specific autophagic elimination of mitochondria.\nMitophagy controls the quality and the number of mitochondria, eliminating dysfunctional or excessive\nmitochondria that can generate reactive oxygen species (ROS) and cause cell death. Mitochondria are centrally\nimplicated in neuron and tissue injury after stroke, due to the function of supplying adenosine triphosphate (ATP)\nto the tissue, regulating oxidative metabolism during the pathologic process, and contribution to apoptotic cell\ndeath after stroke. As a catabolic mechanism, mitophagy links numbers of a complex network of mitochondria, and\naffects mitochondrial dynamic process, fusion and fission, reducing mitochondrial production of ROS, mediated by\nthe mitochondrial permeability transition pore (MPTP). The precise nature of mitophagyâ??s involvement in stroke, and\nits underlying molecular mechanisms, have yet to be fully clarified. This review aims to provide a comprehensive\noverview of the integration of mitochondria with mitophagy, also to introduce and discuss recent advances in the\nunderstanding of the potential role, and possible signaling pathway, of mitophagy in the pathological processes of\nboth hemorrhagic and ischemic stroke. The author also provides evidence to explain the dual role of mitophagy in\nstroke.
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