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- W2118040247 abstract "Normal axonal mitochondrial transport and function is essential for the maintenance of synaptic function. Abnormal mitochondrial motility and mitochondrial dysfunction within axons are critical for amyloid β (Aβ)-induced synaptic stress and the loss of synapses relevant to the pathogenesis of Alzheimer's disease (AD). However, the mechanisms controlling axonal mitochondrial function and transport alterations in AD remain elusive. Here, we report an unexplored role of cyclophilin D (CypD)-dependent mitochondrial permeability transition pore (mPTP) in Aβ-impaired axonal mitochondrial trafficking. Depletion of CypD significantly protects axonal mitochondrial motility and dynamics from Aβ toxicity as shown by increased axonal mitochondrial density and distribution and improved bidirectional transport of axonal mitochondria. Notably, blockade of mPTP by genetic deletion of CypD suppresses Aβ-mediated activation of the p38 mitogen-activated protein kinase signaling pathway, reverses axonal mitochondrial abnormalities, improves synaptic function, and attenuates loss of synapse, suggesting a role of CypD-dependent signaling in Aβ-induced alterations in axonal mitochondrial trafficking. The potential mechanisms of the protective effects of lacking CypD on Aβ-induced abnormal mitochondrial transport in axon are increased axonal calcium buffer capability, diminished reactive oxygen species (ROS), and suppressing downstream signal transduction P38 activation. These findings provide new insights into CypD-dependent mitochondrial mPTP and signaling on mitochondrial trafficking in axons and synaptic degeneration in an environment enriched for Aβ." @default.
- W2118040247 created "2016-06-24" @default.
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- W2118040247 date "2013-01-31" @default.
- W2118040247 modified "2023-10-05" @default.
- W2118040247 title "Cyclophilin D Deficiency Rescues Axonal Mitochondrial Transport in Alzheimer’s Neurons" @default.
- W2118040247 cites W1479749658 @default.
- W2118040247 cites W1967464308 @default.
- W2118040247 cites W1968257316 @default.
- W2118040247 cites W1969853133 @default.
- W2118040247 cites W1970150099 @default.
- W2118040247 cites W1973363462 @default.
- W2118040247 cites W1975428625 @default.
- W2118040247 cites W1986559032 @default.
- W2118040247 cites W1987674607 @default.
- W2118040247 cites W1989331957 @default.
- W2118040247 cites W1993696187 @default.
- W2118040247 cites W1993940179 @default.
- W2118040247 cites W1996764498 @default.
- W2118040247 cites W1996981671 @default.
- W2118040247 cites W1997729278 @default.
- W2118040247 cites W1998118411 @default.
- W2118040247 cites W2002972453 @default.
- W2118040247 cites W2006925676 @default.
- W2118040247 cites W2013690402 @default.
- W2118040247 cites W2015426193 @default.
- W2118040247 cites W2015497527 @default.
- W2118040247 cites W2022959250 @default.
- W2118040247 cites W2025764899 @default.
- W2118040247 cites W2030113770 @default.
- W2118040247 cites W2037801678 @default.
- W2118040247 cites W2039409049 @default.
- W2118040247 cites W2040819167 @default.
- W2118040247 cites W2045085957 @default.
- W2118040247 cites W2045270516 @default.
- W2118040247 cites W2046068037 @default.
- W2118040247 cites W2051690270 @default.
- W2118040247 cites W2054828537 @default.
- W2118040247 cites W2056907950 @default.
- W2118040247 cites W2061091844 @default.
- W2118040247 cites W2062628622 @default.
- W2118040247 cites W2063099262 @default.
- W2118040247 cites W2063936188 @default.
- W2118040247 cites W2065306196 @default.
- W2118040247 cites W2069796133 @default.
- W2118040247 cites W2074655805 @default.
- W2118040247 cites W2074800090 @default.
- W2118040247 cites W2080225612 @default.
- W2118040247 cites W2089521856 @default.
- W2118040247 cites W2098024573 @default.
- W2118040247 cites W2099890622 @default.
- W2118040247 cites W2102518602 @default.
- W2118040247 cites W2103024032 @default.
- W2118040247 cites W2105442740 @default.
- W2118040247 cites W2108386295 @default.
- W2118040247 cites W2108690001 @default.
- W2118040247 cites W2112546324 @default.
- W2118040247 cites W2114633186 @default.
- W2118040247 cites W2116650656 @default.
- W2118040247 cites W2119808485 @default.
- W2118040247 cites W2119983609 @default.
- W2118040247 cites W2124955411 @default.
- W2118040247 cites W2129609456 @default.
- W2118040247 cites W2129971794 @default.
- W2118040247 cites W2130508542 @default.
- W2118040247 cites W2133103790 @default.
- W2118040247 cites W2133631618 @default.
- W2118040247 cites W2134155110 @default.
- W2118040247 cites W2145482520 @default.
- W2118040247 cites W2148999943 @default.
- W2118040247 cites W2152913938 @default.
- W2118040247 cites W2153456027 @default.
- W2118040247 cites W2154874158 @default.
- W2118040247 cites W2156682516 @default.
- W2118040247 cites W2163360776 @default.
- W2118040247 cites W2163757074 @default.
- W2118040247 cites W2165298830 @default.
- W2118040247 cites W2165601218 @default.
- W2118040247 cites W2172651031 @default.
- W2118040247 cites W4323874225 @default.
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- W2118040247 doi "https://doi.org/10.1371/journal.pone.0054914" @default.
- W2118040247 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3561411" @default.
- W2118040247 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/23382999" @default.
- W2118040247 hasPublicationYear "2013" @default.
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