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Ruiz Ojeda, F.J. ; Méndez-Gutiérrez, A.* ; Aguilera, C.M.* ; Plaza-Díaz, J.*

Extracellular matrix remodeling of adipose Ttssue in obesity and metabolic diseases.

Int. J. Mol. Sci. 20:4888 (2019)
Verlagsversion DOI PMC
Open Access Gold
Creative Commons Lizenzvertrag
The extracellular matrix (ECM) is a network of different proteins and proteoglycans that controls differentiation, migration, repair, survival, and development, and it seems that its remodeling is required for healthy adipose tissue expansion. Obesity drives an excessive lipid accumulation in adipocytes, which provokes immune cells infiltration, fibrosis (an excess of deposition of ECM components such as collagens, elastin, and fibronectin) and inflammation, considered a consequence of local hypoxia, and ultimately insulin resistance. To understand the mechanism of this process is a challenge to treat the metabolic diseases. This review is focused at identifying the putative role of ECM in adipose tissue, describing its structure and components, its main tissue receptors, and how it is affected in obesity, and subsequently the importance of an appropriate ECM remodeling in adipose tissue expansion to prevent metabolic diseases.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Review
Schlagwörter Obesity ; Adipose Tissue ; Extracellular Matrix ; Insulin Resistance; Fatty Liver-disease; Muscle Insulin-resistance; Diet-induced Obesity; Body-mass Index; Differential Expression; Therapeutic Targets; Lipid-metabolism; Vascular-disease; Adipocyte Number; Potential Role
Sprache
Veröffentlichungsjahr 2019
HGF-Berichtsjahr 2019
ISSN (print) / ISBN 1661-6596
e-ISSN 1422-0067
Zeitschrift International Journal of Molecular Sciences
Quellenangaben Band: 20, Heft: 19, Seiten: , Artikelnummer: 4888 Supplement: ,
Verlag MDPI
Verlagsort Basel
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Diabetes and Obesity (IDO)
POF Topic(s) 30502 - Diabetes: Pathophysiology, Prevention and Therapy
Forschungsfeld(er) Helmholtz Diabetes Center
PSP-Element(e) G-553400-001
DOI 10.3390/ijms20194888
WOS ID WOS:000494798300229
Scopus ID 85072914011
PubMed ID 31581657
Erfassungsdatum 2019-10-07
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