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001-es BibID:BIBFORM103076
035-os BibID:(WOS)000275563300017 (Scopus)76349105718
Első szerző:Prieur, Xavier
Cím:Lipotoxicity in macrophages: evidence from diseases associated with the metabolic syndrome / Xavier Prieur, Tamás Rőszer, Mercedes Ricote
Dátum:2010
ISSN:1388-1981
Megjegyzések:Accumulation of lipid metabolites within non-adipose tissues can induce chronic inflammation by promoting macrophage infiltration and activation. Oxidized and glycated lipoproteins, free fatty acids, free cholesterol, triacylglycerols, diacylglycerols and ceramides have long been known to induce cellular dysfunction through their pro-inflammatory and pro-apoptotic properties. Emerging evidence suggests that macrophage activation by lipid metabolites and further modulation by lipid signaling represents a common pathogenic mechanism underlying lipotoxicity in atherosclerosis, obesity-associated insulin resistance and inflammatory diseases related to metabolic syndrome such as liver steatosis and chronic kidney disease. In this review, we discuss the latest discoveries that support the role of lipids in modulating the macrophage phenotype in different metabolic diseases. We describe the common mechanisms by which lipid derivatives, through modulation of macrophage function, promote plaque instability in the arterial wall, impair insulin responsiveness and contribute to inflammatory liver, muscle and kidney disease. We discuss the molecular mechanism of lipid activation of pro-inflammatory pathways (JNK, NF kappa B) and the key roles played by the PPAR and LXR nuclear receptors-lipid sensors that link lipid metabolism and inflammation.
Tárgyszavak:Természettudományok Biológiai tudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Lipotoxicity
Macrophage
Nuclear receptor
Inflammation
Insulin resistance
Atherosclerosis
Megjelenés:Biochimica et Biophysica Acta (BBA). Molecular and Cell Biology of Lipids. - 1801 : 3 (2010), p. 327-337. -
További szerzők:Röszer Tamás (1979-) (orvos, biológus) Ricote, Mercedes
Pályázati támogatás:OTKA-76091
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