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Proteostasis in thermogenesis and obesity.
Biol. Chem. 401, 1019-1030 (2020)
The proper production, degradation, folding and activity of proteins, proteostasis, is essential for any cellular function. From single cell organisms to humans, selective pressures have led to the evolution of adaptive programs that ensure proteins are properly produced and disposed of when necessary. Environmental factors such as temperature, nutrient availability, pathogens as well as predators have greatly influenced the development of mechanisms such as the unfolded protein response, endoplasmic reticulum-associated protein degradation and autophagy, working together in concert to secure cellular proteostasis. In our modern society, the metabolic systems of the human body face the distinct challenge of changed diets, chronic overnutrition and sedentary lifestyles. Obesity and excess white adipose tissue accumulation are linked to a cluster of metabolic diseases and disturbed proteostasis is a common feature. Conversely, processes that promote energy expenditure such as exercise, shivering as well as non-shivering thermogenesis by brown adipose tissue (BAT) and beige adipocytes counter-act metabolic dysfunction. Here we review the basic concepts of proteostasis in obesity-linked metabolic diseases and focus on adipocytes, which are critical regulators of mammalian energy metabolism.
Impact Factor
Scopus SNIP
Web of Science
Times Cited
Times Cited
Scopus
Cited By
Cited By
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3.270
0.789
6
10
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Publication type
Article: Journal article
Document type
Review
Keywords
Adipocyte ; Endoplasmic Reticulum ; Obesity ; Proteostasis ; Thermogenesis; Brown Adipose-tissue; Endoplasmic-reticulum Stress; Unfolded Protein Response; Transcription Factor; Er Stress; Proteasomal Degradation; Insulin-resistance; Links Obesity; Mechanisms; Adipocytes
Language
english
Publication Year
2020
Prepublished in Year
2019
HGF-reported in Year
2019
ISSN (print) / ISBN
1431-6730
e-ISSN
1437-4315
Journal
Biological Chemistry
Quellenangaben
Volume: 401,
Issue: 9,
Pages: 1019-1030
Publisher
de Gruyter
Publishing Place
Genthiner Strasse 13, D-10785 Berlin, Germany
Reviewing status
Peer reviewed
Institute(s)
Institute of Diabetes and Cancer (IDC)
POF-Topic(s)
90000 - German Center for Diabetes Research
Research field(s)
Helmholtz Diabetes Center
PSP Element(s)
G-501900-251
WOS ID
WOS:000560516600002
Scopus ID
85081387219
PubMed ID
32061163
Erfassungsdatum
2020-03-24