2026-06-30T02:01:11Zhttps://repisalud.isciii.es/rest/oai/requestoai:repisalud.isciii.es:20.500.12105/78782024-11-29T16:36:37Zcom_20.500.12105_2173com_20.500.12105_2051col_20.500.12105_19597
Repisalud
author
Petruzzelli, Michele
author
Wagner, Erwin Friedrich
funder
Unión Europea. Comisión Europea. European Research Council (ERC)
funder
Ministerio de Economía y Competitividad (España)
2019-07-10T09:01:38Z
2019-07-10T09:01:38Z
2016-03-01
Genes Dev. 2016;30(5):489-501.
10.1101/gad.276733.115
1549-5477
0890-9369
Genes & development
26944676
http://hdl.handle.net/20.500.12105/7878
Metabolic dysfunction contributes to the clinical deterioration observed in advanced cancer patients and is characterized by weight loss, skeletal muscle wasting, and atrophy of the adipose tissue. This systemic syndrome, termed cancer-associated cachexia (CAC), is a major cause of morbidity and mortality. While once attributed solely to decreased food intake, the present description of cancer cachexia is a disorder of multiorgan energy imbalance. Here we review the molecules and pathways responsible for metabolic dysfunction in CAC and the ideas that led to the current understanding.
eng
cancer-associated cachexia (CAC)
metabolic failure
skeletal muscle atrophy
white adipose tissue (WAT) browning
Mechanisms of metabolic dysfunction in cancer-associated cachexia
journal article
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URL
https://repisalud.isciii.es/bitstreams/ccaa6a5b-d77f-4a6a-a47e-6a795b9fde49/download
File
MD5
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application/pdf
Mechanismsofmetabolicdysfunction_2016.pdf
URL
https://repisalud.isciii.es/bitstreams/db3200b1-e13c-4d1c-bdd1-79a2f92250cc/download
File
MD5
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text/plain
Mechanismsofmetabolicdysfunction_2016.pdf.txt