Mitochondrial autophagy(mitophagy)is the selective clearance of damaged or incomplete mitochondria by autophagy,which is critical for the functional integrity of the entire mitochondrial network and cell survival.Beca...Mitochondrial autophagy(mitophagy)is the selective clearance of damaged or incomplete mitochondria by autophagy,which is critical for the functional integrity of the entire mitochondrial network and cell survival.Because dysfunction of mitophagy is closely related to many diseases,it is important to study the specific molecular mechanism and pathophysiological significance of mitophagy.FUN14 domain-containing 1(FUNDC1)is a newly identified mitochon-drial outer membrane protein that induces receptor-mediated mitophagy by its interaction with LC3 during hypoxia.The expression,phosphorylation,regulation and significance of FUNDC1 are reviewed in the context of a large number of pathophysiological conditions.Emerging evidence has demonstrated that levels and phosphorylation states of FUNDC1 are closely related to occur-rence,progression and prognosis of various diseases including heart diseases and cancers,indi-cating that FUNDC1 may serve as a promising biomarker and potential therapeutic target.展开更多
In light of the accelerated aging of the global population and the deterioration of the atmosphere pollution, we sought to clarify the potential mechanisms by which fine particulate matter（PM_（2.5）） can cause cogn...In light of the accelerated aging of the global population and the deterioration of the atmosphere pollution, we sought to clarify the potential mechanisms by which fine particulate matter（PM_（2.5）） can cause cognitive impairment and neurodegeneration through the alteration of mitochondrial structure and function. The results indicate that PM_（2.5） inhalation reduces ATP production by disrupting the aerobic tricarboxylic acid cycle and oxidative phosphorylation, thereby causing the hypophosphorylation of tau in the cortices of middle-aged mice. Furthermore, excessive reactive oxygen species generation was involved in the impairment. Interestingly, these alterations were partially reversed after exposure to PM_（2.5） ended. These findings clarify the mechanism involved in mitochondrial abnormality-related neuropathological dysfunction in response to atmospheric PM_（2.5） inhalation and provide an optimistic sight for alleviating the adverse health outcomes in polluted areas.展开更多
基金This research was supported by the Natural Science Foun-dation of China[grant number 31871392]the Beijing Natural Science Foundation[grant number 5192014]+1 种基金China postdoctoral[grant number 2013 M541041]Weilin Zhang.Weilin Zhang is a recipient of the Innovation Foun-dation of Beijing University of Aeronautics and Astronautics(BUAA)and the Academic Innovation Award of Ministry of Education[grant number 401059].
文摘Mitochondrial autophagy(mitophagy)is the selective clearance of damaged or incomplete mitochondria by autophagy,which is critical for the functional integrity of the entire mitochondrial network and cell survival.Because dysfunction of mitophagy is closely related to many diseases,it is important to study the specific molecular mechanism and pathophysiological significance of mitophagy.FUN14 domain-containing 1(FUNDC1)is a newly identified mitochon-drial outer membrane protein that induces receptor-mediated mitophagy by its interaction with LC3 during hypoxia.The expression,phosphorylation,regulation and significance of FUNDC1 are reviewed in the context of a large number of pathophysiological conditions.Emerging evidence has demonstrated that levels and phosphorylation states of FUNDC1 are closely related to occur-rence,progression and prognosis of various diseases including heart diseases and cancers,indi-cating that FUNDC1 may serve as a promising biomarker and potential therapeutic target.
基金supported by the National Science Foundation of China(Nos.21377076,91543203,21477070,21222701)Specialized Research Fund for the Doctoral Program of Higher Education of China(Nos.20121401110003,20131401110005)+1 种基金Project Supported by Shanxi Young Sanjin Scholarship of China,Program for the Outstanding Innovative Teams of Higher Learning Institutions of ShanxiResearch Project Supported by Shanxi Scholarship Council of China(No.2015-006)
文摘In light of the accelerated aging of the global population and the deterioration of the atmosphere pollution, we sought to clarify the potential mechanisms by which fine particulate matter（PM_（2.5）） can cause cognitive impairment and neurodegeneration through the alteration of mitochondrial structure and function. The results indicate that PM_（2.5） inhalation reduces ATP production by disrupting the aerobic tricarboxylic acid cycle and oxidative phosphorylation, thereby causing the hypophosphorylation of tau in the cortices of middle-aged mice. Furthermore, excessive reactive oxygen species generation was involved in the impairment. Interestingly, these alterations were partially reversed after exposure to PM_（2.5） ended. These findings clarify the mechanism involved in mitochondrial abnormality-related neuropathological dysfunction in response to atmospheric PM_（2.5） inhalation and provide an optimistic sight for alleviating the adverse health outcomes in polluted areas.
