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1000 Titel
  • Sarcopenia – Molecular mechanisms and open questions
1000 Autor/in
  1. Wiedmer, Petra |
  2. Jung, Tobias |
  3. Castro, José Pedro |
  4. Pomatto, Laura C. D. |
  5. Sun, Patrick Y. |
  6. Davies, Kelvin J. A. |
  7. Grune, Tilman |
1000 Erscheinungsjahr 2020
1000 LeibnizOpen
1000 Publikationstyp
  1. Artikel |
1000 Online veröffentlicht
  • 2020-10-29
1000 Erschienen in
1000 Quellenangabe
  • 65:101200
1000 FRL-Sammlung
1000 Copyrightjahr
  • 2020
1000 Lizenz
1000 Verlagsversion
  • https://doi.org/10.1016/j.arr.2020.101200 |
1000 Publikationsstatus
1000 Begutachtungsstatus
1000 Sprache der Publikation
1000 Abstract/Summary
  • Sarcopenia represents a muscle-wasting syndrome characterized by progressive and generalized degenerative loss of skeletal muscle mass, quality, and strength occurring during normal aging. Sarcopenia patients are mainly suffering from the loss in muscle strength and are faced with mobility disorders reducing their quality of life and are, therefore, at higher risk for morbidity (falls, bone fracture, metabolic diseases) and mortality. Several molecular mechanisms have been described as causes for sarcopenia that refer to very different levels of muscle physiology. These mechanisms cover e. g. function of hormones (e. g. IGF-1 and Insulin), muscle fiber composition and neuromuscular drive, myo-satellite cell potential to differentiate and proliferate, inflammatory pathways as well as intracellular mechanisms in the processes of proteostasis and mitochondrial function. In this review, we describe sarcopenia as a muscle-wasting syndrome distinct from other atrophic diseases and summarize the current view on molecular causes of sarcopenia development as well as open questions provoking further research efforts for establishing efficient lifestyle and therapeutic interventions.
1000 Sacherschließung
lokal Mitochondria, Muscle fibre composition
lokal Proteostasis
lokal Proteasome
lokal Autophagy
lokal Molecular pathways
1000 Fächerklassifikation (DDC)
1000 Liste der Beteiligten
  1. https://frl.publisso.de/adhoc/uri/V2llZG1lciwgUGV0cmE=|https://frl.publisso.de/adhoc/uri/SnVuZywgVG9iaWFz|https://frl.publisso.de/adhoc/uri/Q2FzdHJvLCBKb3PDqSBQZWRybw==|https://frl.publisso.de/adhoc/uri/UG9tYXR0bywgTGF1cmEgQy4gRC4=|https://frl.publisso.de/adhoc/uri/U3VuLCBQYXRyaWNrIFku|https://frl.publisso.de/adhoc/uri/RGF2aWVzLCBLZWx2aW4gSi4gQS4=|https://frl.publisso.de/adhoc/uri/R3J1bmUsIFRpbG1hbg==
1000 Label
1000 Förderer
  1. National Institute of Environmental Health Sciences |
  2. National Institute on Aging |
  3. Deutsche Forschungsgemeinschaft |
  4. Seventh Framework Programme |
1000 Fördernummer
  1. ES003598
  2. AG052374
  3. GR1240/20-1; GR 1240/22-1
  4. -
1000 Förderprogramm
  1. -
  2. -
  3. -
  4. consortium FRAILOMIC
1000 Dateien
  1. Sarcopenia – Molecular mechanisms and open questions
1000 Förderung
  1. 1000 joinedFunding-child
    1000 Förderer National Institute of Environmental Health Sciences |
    1000 Förderprogramm -
    1000 Fördernummer ES003598
  2. 1000 joinedFunding-child
    1000 Förderer National Institute on Aging |
    1000 Förderprogramm -
    1000 Fördernummer AG052374
  3. 1000 joinedFunding-child
    1000 Förderer Deutsche Forschungsgemeinschaft |
    1000 Förderprogramm -
    1000 Fördernummer GR1240/20-1; GR 1240/22-1
  4. 1000 joinedFunding-child
    1000 Förderer Seventh Framework Programme |
    1000 Förderprogramm consortium FRAILOMIC
    1000 Fördernummer -
1000 Objektart article
1000 Beschrieben durch
1000 @id frl:6427780.rdf
1000 Erstellt am 2021-05-28T11:27:23.474+0200
1000 Erstellt von 25
1000 beschreibt frl:6427780
1000 Bearbeitet von 25
1000 Zuletzt bearbeitet Fri May 28 11:29:53 CEST 2021
1000 Objekt bearb. Fri May 28 11:29:12 CEST 2021
1000 Vgl. frl:6427780
1000 Oai Id
  1. oai:frl.publisso.de:frl:6427780 |
1000 Sichtbarkeit Metadaten public
1000 Sichtbarkeit Daten public
1000 Gegenstand von

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