FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2891525455> ?p ?o ?g. }

• W2891525455 endingPage "e0203630" @default.
• W2891525455 startingPage "e0203630" @default.
• W2891525455 abstract "Hypoxemia in humans may occur during high altitude mountaineering and in patients suffering from ventilatory insufficiencies such as cardiovascular- or respiratory disease including Chronic Obstructive Pulmonary Disease (COPD). In these conditions, hypoxemia has been correlated to reduced appetite and decreased food intake. Since hypoxemia and reduced food intake intersect in various physiological and pathological conditions and both induce loss of muscle mass, we investigated whether hypoxia aggravates fasting-induced skeletal muscle atrophy and evaluated underlying protein turnover signaling.Mice were kept under hypoxic (8% oxygen) or normoxic conditions (21% oxygen), or were pair-fed to the hypoxia group for 12 days. Following an additional 24 hours of fasting, muscle weight and protein turnover signaling were assessed in the gastrocnemius muscle by RT-qPCR and Western blotting.Loss of gastrocnemius muscle mass in response to fasting in the hypoxic group was increased compared to the normoxic group, but not to the pair-fed normoxic control group. Conversely, the fasting-induced increase in poly-ubiquitin conjugation, and expression of the ubiquitin 26S-proteasome E3 ligases, autophagy-lysosomal degradation-related mRNA transcripts and proteins, and markers of the integrated stress response (ISR), were attenuated in the hypoxia group compared to the pair-fed group. Mammalian target of rapamycin complex 1 (mTORC1) downstream signaling was reduced by fasting under normoxic conditions, but sustained under hypoxic conditions. Activation of AMP-activated protein kinase (AMPK) / tuberous sclerosis complex 2 (TSC2) signaling by fasting was absent, in line with retained mTORC1 activity under hypoxic conditions. Similarly, hypoxia suppressed AMPK-mediated glucocorticoid receptor (GR) signaling following fasting, which corresponded with blunted proteolytic signaling responses.Hypoxia aggravates fasting-induced muscle wasting, and suppresses AMPK and ISR activation. Altered AMPK-mediated regulation of mTORC1 and GR may underlie aberrant protein turnover signaling and affect muscle atrophy responses in hypoxic skeletal muscle." @default.
• W2891525455 created "2018-09-27" @default.
• W2891525455 creator A5004953111 @default.
• W2891525455 creator A5013717261 @default.
• W2891525455 creator A5036247477 @default.
• W2891525455 creator A5043038636 @default.
• W2891525455 creator A5047602412 @default.
• W2891525455 creator A5052827329 @default.
• W2891525455 date "2018-09-13" @default.
• W2891525455 modified "2023-09-26" @default.
• W2891525455 title "Hypoxia impairs adaptation of skeletal muscle protein turnover- and AMPK signaling during fasting-induced muscle atrophy" @default.
• W2891525455 cites W1266576439 @default.
• W2891525455 cites W1506261045 @default.
• W2891525455 cites W1523693806 @default.
• W2891525455 cites W1578146465 @default.
• W2891525455 cites W1848960512 @default.
• W2891525455 cites W191098488 @default.
• W2891525455 cites W1943424262 @default.
• W2891525455 cites W1970637701 @default.
• W2891525455 cites W1972542282 @default.
• W2891525455 cites W1973307538 @default.
• W2891525455 cites W1976643149 @default.
• W2891525455 cites W1977925028 @default.
• W2891525455 cites W1984392799 @default.
• W2891525455 cites W1989307078 @default.
• W2891525455 cites W2002226709 @default.
• W2891525455 cites W2007534790 @default.
• W2891525455 cites W2014425292 @default.
• W2891525455 cites W2016712537 @default.
• W2891525455 cites W2016752484 @default.
• W2891525455 cites W2019795235 @default.
• W2891525455 cites W2024879415 @default.
• W2891525455 cites W2025192214 @default.
• W2891525455 cites W2029769474 @default.
• W2891525455 cites W2031308904 @default.
• W2891525455 cites W2033328537 @default.
• W2891525455 cites W2033797333 @default.
• W2891525455 cites W2035397862 @default.
• W2891525455 cites W2036681631 @default.
• W2891525455 cites W2038582177 @default.
• W2891525455 cites W2039328837 @default.
• W2891525455 cites W2059055543 @default.
• W2891525455 cites W2061825971 @default.
• W2891525455 cites W2070871404 @default.
• W2891525455 cites W2078561735 @default.
• W2891525455 cites W2079936381 @default.
• W2891525455 cites W2079961758 @default.
• W2891525455 cites W2080447685 @default.
• W2891525455 cites W2081305406 @default.
• W2891525455 cites W2086729364 @default.
• W2891525455 cites W2087648632 @default.
• W2891525455 cites W2088832303 @default.
• W2891525455 cites W2090966736 @default.
• W2891525455 cites W2097634421 @default.
• W2891525455 cites W2100688137 @default.
• W2891525455 cites W2101050876 @default.
• W2891525455 cites W2103628478 @default.
• W2891525455 cites W2107045511 @default.
• W2891525455 cites W2107536472 @default.
• W2891525455 cites W2113288593 @default.
• W2891525455 cites W2115160479 @default.
• W2891525455 cites W2127951128 @default.
• W2891525455 cites W2130396048 @default.
• W2891525455 cites W2130684621 @default.
• W2891525455 cites W2134675753 @default.
• W2891525455 cites W2135502283 @default.
• W2891525455 cites W2148954658 @default.
• W2891525455 cites W2152295887 @default.
• W2891525455 cites W2153903825 @default.
• W2891525455 cites W2153950719 @default.
• W2891525455 cites W2158535498 @default.
• W2891525455 cites W2160488228 @default.
• W2891525455 cites W2161580614 @default.
• W2891525455 cites W2167033587 @default.
• W2891525455 cites W2167512318 @default.
• W2891525455 cites W2170159157 @default.
• W2891525455 cites W2170362894 @default.
• W2891525455 cites W2187297855 @default.
• W2891525455 cites W2315543056 @default.
• W2891525455 cites W2317307850 @default.
• W2891525455 cites W2317908925 @default.
• W2891525455 cites W2356537477 @default.
• W2891525455 cites W2400936627 @default.
• W2891525455 cites W2518959324 @default.
• W2891525455 cites W2524762117 @default.
• W2891525455 cites W2571424615 @default.
• W2891525455 doi "https://doi.org/10.1371/journal.pone.0203630" @default.
• W2891525455 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6136752" @default.
• W2891525455 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30212583" @default.
• W2891525455 hasPublicationYear "2018" @default.
• W2891525455 type Work @default.
• W2891525455 sameAs 2891525455 @default.
• W2891525455 citedByCount "12" @default.
• W2891525455 countsByYear W28915254552019 @default.
• W2891525455 countsByYear W28915254552020 @default.
• W2891525455 countsByYear W28915254552021 @default.
• W2891525455 countsByYear W28915254552022 @default.
• W2891525455 countsByYear W28915254552023 @default.

• next