Matches in SemOpenAlex for { <https://semopenalex.org/work/W2904605547> ?p ?o ?g. }
- W2904605547 abstract "Skeletal muscle is a dynamic tissue capable of responding to a large variety of physiological stimuli by adjusting muscle fiber size, metabolism and function. However, in pathological conditions such as cancer and neural disorders, this finely regulated homeostasis is impaired leading to severe muscle wasting, reduced muscle fiber size (atrophy), and impaired function. These disease features develop due to enhanced protein breakdown, which relies on two major degradation systems: the ubiquitin-proteasome and the autophagy-lysosome. These systems are independently regulated by different signalling pathways, which in physiological conditions, determine protein and organelle turnover. However, alterations in one or both systems, as it happens in several disorders, leads to enhanced protein breakdown and muscle atrophy. Although this is a common feature in the different types of muscle atrophy, the relative contribution of each of these systems is still under debate. Here, we will briefly describe the regulation and the activity of the ubiquitin-proteasome and the autophagy-lysosome systems during muscle wasting. We will then discuss what we know regarding how these pathways are involved in cancer induced and in neurogenic muscle atrophy, highlighting common and divergent paths. It is now clear that there is no one unifying common mechanism that can be applied to all models of muscle loss. Detailed understanding of the pathways and proteolysis mechanisms involved in each model will hopefully help the development of drugs to counteract muscle wasting in specific conditions." @default.
- W2904605547 created "2018-12-22" @default.
- W2904605547 creator A5005272488 @default.
- W2904605547 creator A5021622442 @default.
- W2904605547 creator A5040335915 @default.
- W2904605547 creator A5065505549 @default.
- W2904605547 date "2018-12-13" @default.
- W2904605547 modified "2023-10-18" @default.
- W2904605547 title "Do neurogenic and cancer-induced muscle atrophy follow common or divergent paths?" @default.
- W2904605547 cites W1564746483 @default.
- W2904605547 cites W1590405048 @default.
- W2904605547 cites W1590930560 @default.
- W2904605547 cites W1597512020 @default.
- W2904605547 cites W1850103453 @default.
- W2904605547 cites W1850779446 @default.
- W2904605547 cites W1965047073 @default.
- W2904605547 cites W1966333337 @default.
- W2904605547 cites W1973622869 @default.
- W2904605547 cites W1974706622 @default.
- W2904605547 cites W1977695145 @default.
- W2904605547 cites W1979153753 @default.
- W2904605547 cites W1985257308 @default.
- W2904605547 cites W1985534077 @default.
- W2904605547 cites W1993407106 @default.
- W2904605547 cites W1995949259 @default.
- W2904605547 cites W1997014674 @default.
- W2904605547 cites W2004830125 @default.
- W2904605547 cites W2005229247 @default.
- W2904605547 cites W2006545231 @default.
- W2904605547 cites W2014897682 @default.
- W2904605547 cites W2014899456 @default.
- W2904605547 cites W2017969831 @default.
- W2904605547 cites W2019558909 @default.
- W2904605547 cites W2025192214 @default.
- W2904605547 cites W2033797333 @default.
- W2904605547 cites W2035555824 @default.
- W2904605547 cites W2036787961 @default.
- W2904605547 cites W2040691328 @default.
- W2904605547 cites W2042524770 @default.
- W2904605547 cites W2045592436 @default.
- W2904605547 cites W2047439821 @default.
- W2904605547 cites W2052107105 @default.
- W2904605547 cites W2054800877 @default.
- W2904605547 cites W2061929833 @default.
- W2904605547 cites W2073522519 @default.
- W2904605547 cites W2076111143 @default.
- W2904605547 cites W2081305406 @default.
- W2904605547 cites W2082092138 @default.
- W2904605547 cites W2084860871 @default.
- W2904605547 cites W2088975007 @default.
- W2904605547 cites W2090950464 @default.
- W2904605547 cites W2100178504 @default.
- W2904605547 cites W2100688137 @default.
- W2904605547 cites W2107867413 @default.
- W2904605547 cites W2112956181 @default.
- W2904605547 cites W2113882045 @default.
- W2904605547 cites W2115610308 @default.
- W2904605547 cites W2119068566 @default.
- W2904605547 cites W2119303027 @default.
- W2904605547 cites W2129034320 @default.
- W2904605547 cites W2130053803 @default.
- W2904605547 cites W2135214326 @default.
- W2904605547 cites W2138904483 @default.
- W2904605547 cites W2144203293 @default.
- W2904605547 cites W2144716911 @default.
- W2904605547 cites W2147058114 @default.
- W2904605547 cites W2148527632 @default.
- W2904605547 cites W2149318570 @default.
- W2904605547 cites W2150059080 @default.
- W2904605547 cites W2157644555 @default.
- W2904605547 cites W2159101355 @default.
- W2904605547 cites W2159796957 @default.
- W2904605547 cites W2160273104 @default.
- W2904605547 cites W2162063376 @default.
- W2904605547 cites W2162434225 @default.
- W2904605547 cites W2165957291 @default.
- W2904605547 cites W2167033587 @default.
- W2904605547 cites W2167512318 @default.
- W2904605547 cites W2167872252 @default.
- W2904605547 cites W2168492534 @default.
- W2904605547 cites W2169448756 @default.
- W2904605547 cites W2171103810 @default.
- W2904605547 cites W2171726169 @default.
- W2904605547 cites W2219305167 @default.
- W2904605547 cites W2285784867 @default.
- W2904605547 cites W2320366000 @default.
- W2904605547 cites W2408786519 @default.
- W2904605547 cites W2461444254 @default.
- W2904605547 cites W2478304422 @default.
- W2904605547 cites W2505633754 @default.
- W2904605547 cites W2522369681 @default.
- W2904605547 cites W2602865457 @default.
- W2904605547 cites W2752326209 @default.
- W2904605547 cites W2788414515 @default.
- W2904605547 cites W2795170199 @default.
- W2904605547 cites W2805909146 @default.
- W2904605547 cites W2885919710 @default.
- W2904605547 cites W2891303753 @default.
- W2904605547 cites W30273463 @default.
- W2904605547 doi "https://doi.org/10.4081/ejtm.2018.7931" @default.