Mitophagy, a potential therapeutic target for stroke View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2018-12

AUTHORS

Ruiqiao Guan, Wei Zou, Xiaohong Dai, Xueping Yu, Hao Liu, Qiuxin Chen, Wei Teng

ABSTRACT

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

PAGES

87

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1186/s12929-018-0487-4

    DOI

    http://dx.doi.org/10.1186/s12929-018-0487-4

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1110281456

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/30501621


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