FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2800843754> ?p ?o ?g. }

• W2800843754 abstract "Parkin is a ubiquitin ligase that is involved in the selective removal of dysfunctional mitochondria. This process is termed mitophagy and can assist in mitochondrial quality control. Endurance training can produce adaptations in skeletal muscle toward a more oxidative phenotype, an outcome of enhanced mitochondrial biogenesis. It remains unknown whether Parkin-mediated mitophagy is involved in training-induced increases in mitochondrial content and function. Our purpose was to determine a role for Parkin in maintaining mitochondrial turnover in muscle, and its requirement in mediating mitochondrial biogenesis following endurance exercise training.Wild-type and Parkin knockout (KO) mice were trained for 6 weeks and then treated with colchicine or vehicle to evaluate the role of Parkin in mediating changes in mitochondrial content, function and acute exercise-induced mitophagy flux.Our results indicate that Parkin is required for the basal maintenance of mitochondrial function. The absence of Parkin did not significantly alter mitophagy basally; however, acute exercise produced an elevation in mitophagy flux, a response that was Parkin-dependent. Mitochondrial content was increased following training in both genotypes, but this occurred without an induction of PGC-1α signaling in KO animals. Interestingly, the increased muscle mitochondrial content in response to training did not influence basal mitophagy flux, despite an enhanced expression and localization of Parkin to mitochondria in WT animals. Furthermore, exercise-induced mitophagy flux was attenuated with training in WT animals, suggesting a lower rate of mitochondrial degradation resulting from improved organelle quality with training. In contrast, training led to a higher mitochondrial content, but with persistent dysfunction, in KO animals. Thus, the lack of a rescue of mitochondrial dysfunction with training in the absence of Parkin is the likely reason for the impaired training-induced attenuation of mitophagy flux compared to WT animals.Our study demonstrates that Parkin is required for exercise-induced mitophagy flux. Exercise-induced mitophagy is reduced with training in muscle, likely due to attenuated signaling consequent to increased mitochondrial content and quality. Our data suggest that Parkin is essential for the maintenance of basal mitochondrial function, as well as for the accumulation of normally functioning mitochondria as a result of training adaptations in muscle." @default.
• W2800843754 created "2018-05-17" @default.
• W2800843754 creator A5027560904 @default.
• W2800843754 creator A5076563879 @default.
• W2800843754 creator A5083848404 @default.
• W2800843754 date "2018-03-17" @default.
• W2800843754 modified "2023-10-17" @default.
• W2800843754 title "Role of Parkin and endurance training on mitochondrial turnover in skeletal muscle" @default.
• W2800843754 cites W1523693806 @default.
• W2800843754 cites W1527237994 @default.
• W2800843754 cites W1566648241 @default.
• W2800843754 cites W1582080277 @default.
• W2800843754 cites W1615913434 @default.
• W2800843754 cites W1926228770 @default.
• W2800843754 cites W1957983000 @default.
• W2800843754 cites W1988276481 @default.
• W2800843754 cites W1989305503 @default.
• W2800843754 cites W1994408958 @default.
• W2800843754 cites W1995381409 @default.
• W2800843754 cites W2000301075 @default.
• W2800843754 cites W2007997420 @default.
• W2800843754 cites W2011951281 @default.
• W2800843754 cites W2014918593 @default.
• W2800843754 cites W2015397524 @default.
• W2800843754 cites W2022997027 @default.
• W2800843754 cites W2024782183 @default.
• W2800843754 cites W2032382748 @default.
• W2800843754 cites W2033515464 @default.
• W2800843754 cites W2034087770 @default.
• W2800843754 cites W2038834667 @default.
• W2800843754 cites W2041198637 @default.
• W2800843754 cites W2041386167 @default.
• W2800843754 cites W2043276141 @default.
• W2800843754 cites W2046440697 @default.
• W2800843754 cites W2049175236 @default.
• W2800843754 cites W2051240076 @default.
• W2800843754 cites W2052889619 @default.
• W2800843754 cites W2055124287 @default.
• W2800843754 cites W2057057259 @default.
• W2800843754 cites W2057731584 @default.
• W2800843754 cites W2063247785 @default.
• W2800843754 cites W2065234142 @default.
• W2800843754 cites W2067097574 @default.
• W2800843754 cites W2075557750 @default.
• W2800843754 cites W2076598575 @default.
• W2800843754 cites W2080270879 @default.
• W2800843754 cites W2082425146 @default.
• W2800843754 cites W2082476985 @default.
• W2800843754 cites W2087592289 @default.
• W2800843754 cites W2088962120 @default.
• W2800843754 cites W2092236266 @default.
• W2800843754 cites W2102136953 @default.
• W2800843754 cites W2106444069 @default.
• W2800843754 cites W2107945166 @default.
• W2800843754 cites W2108326484 @default.
• W2800843754 cites W2109123740 @default.
• W2800843754 cites W2114806766 @default.
• W2800843754 cites W2119399459 @default.
• W2800843754 cites W2120348861 @default.
• W2800843754 cites W2123065811 @default.
• W2800843754 cites W2128705476 @default.
• W2800843754 cites W2129826948 @default.
• W2800843754 cites W2135767505 @default.
• W2800843754 cites W2137651420 @default.
• W2800843754 cites W2138311396 @default.
• W2800843754 cites W2140647923 @default.
• W2800843754 cites W2146124002 @default.
• W2800843754 cites W2147459821 @default.
• W2800843754 cites W2155015733 @default.
• W2800843754 cites W2158088166 @default.
• W2800843754 cites W2160697936 @default.
• W2800843754 cites W2167867141 @default.
• W2800843754 cites W2171103810 @default.
• W2800843754 cites W2179041531 @default.
• W2800843754 cites W2204029290 @default.
• W2800843754 cites W2223597625 @default.
• W2800843754 cites W2267374287 @default.
• W2800843754 cites W2299724091 @default.
• W2800843754 cites W2301918656 @default.
• W2800843754 cites W2410292096 @default.
• W2800843754 cites W2474050726 @default.
• W2800843754 cites W2517107066 @default.
• W2800843754 cites W2580495962 @default.
• W2800843754 cites W2743254891 @default.
• W2800843754 cites W2755721896 @default.
• W2800843754 doi "https://doi.org/10.1186/s13395-018-0157-y" @default.
• W2800843754 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/5857114" @default.
• W2800843754 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/29549884" @default.
• W2800843754 hasPublicationYear "2018" @default.
• W2800843754 type Work @default.
• W2800843754 sameAs 2800843754 @default.
• W2800843754 citedByCount "73" @default.
• W2800843754 countsByYear W28008437542018 @default.
• W2800843754 countsByYear W28008437542019 @default.
• W2800843754 countsByYear W28008437542020 @default.
• W2800843754 countsByYear W28008437542021 @default.
• W2800843754 countsByYear W28008437542022 @default.
• W2800843754 countsByYear W28008437542023 @default.
• W2800843754 crossrefType "journal-article" @default.
• W2800843754 hasAuthorship W2800843754A5027560904 @default.

• next