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001-es BibID:BIBFORM103072
035-os BibID:(cikkazonosító)219583 (WOS)000278509700001 (Scopus)77953493182
Első szerző:Fuentes, Lucía
Cím:Inflammatory mediators and insulin resistance in obesity : role of nuclear receptor signaling in macrophages / Lucía Fuentes, Tamás Rőszer, Mercedes Ricote
Dátum:2010
ISSN:0962-9351
Megjegyzések:Visceral obesity is coupled to a general low-grade chronic inflammatory state characterized by macrophage activation and inflammatory cytokine production, leading to insulin resistance (IR). The balance between proinflammatory M1 and antiinflammatory M2 macrophage phenotypes within visceral adipose tissue appears to be crucially involved in the development of obesity-associated IR and consequent metabolic abnormalities. The ligand-dependent transcription factors peroxisome proliferator activated receptors (PPARs) have recently been implicated in the determination of the M1/M2 phenotype. Liver X receptors (LXRs), which form another subgroup of the nuclear receptor superfamily, are also important regulators of proinflammatory cytokine production in macrophages. Disregulation of macrophage-mediated inflammation by PPARs and LXRs therefore underlies the development of IR. This review summarizes the role of PPAR and LXR signaling in macrophages and current knowledge about the impact of these actions in the manifestation of IR and obesity comorbidities such as liver steatosis and diabetic osteopenia.
Tárgyszavak:Természettudományok Biológiai tudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Mediators of Inflammation. - 2010 (2010), p. 1-10. -
További szerzők:Röszer Tamás (1979-) (orvos, biológus) Ricote, Mercedes
Pályázati támogatás:OTKA-76091
OTKA
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001-es BibID:BIBFORM103130
035-os BibID:(Wos)000348962700035 (Scopus)84922169574
Első szerző:Menendez-Gutierrez, Maria Piedad
Cím:Retinoid X receptors orchestrate osteoclast differentiation and postnatal bone remodeling / María P. Menéndez-Gutiérrez, Tamás Röszer, Lucia Fuentes, Vanessa Núnez, Amelia Escolano, Juan Miguel Redondo, Nora De Clerk, Daniel Metzger, Annabel F. Valledor, Mercedes Ricote
Dátum:2015
ISSN:0021-9738
Megjegyzések:Osteoclasts are bone-resorbing cells that are important for maintenance of bone remodeling and mineral homeostasis. Regulation of osteoclast differentiation and activity is important for the pathogenesis and treatment of diseases associated with bone loss. Here, we demonstrate that retinoid X receptors (RXRs) are key elements of the transcriptional program of differentiating osteoclasts. Loss of RXR function in hematopoietic cells resulted in formation of giant, nonresorbing osteoclasts and increased bone mass in male mice and protected female mice from bone loss following ovariectomy, which induces osteoporosis in WT females. The increase in bone mass associated with RXR deficiency was due to lack of expression of the RXR-dependent transcription factor v-maf musculoaponeurotic fibrosarcoma oncogene family, protein B (MAFB) in osteoclast progenitors. Evaluation of osteoclast progenitor cells revealed that RXR homodimers directly target and bind to the Mafb promoter, and this interaction is required for proper osteoclast proliferation, differentiation, and activity. Pharmacological activation of RXRs inhibited osteoclast differentiation due to the formation of RXR/liver X receptor (LXR) heterodimers, which induced expression of sterol regulatory element binding protein-1c (SREBP-1c), resulting in indirect MAFB upregulation. Our study reveals that RXR signaling mediates bone homeostasis and suggests that RXRs have potential as targets for the treatment of bone pathologies such as osteoporosis.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Journal Of Clinical Investigation. - 125 : 2 (2015), p.809-823. -
További szerzők:Röszer Tamás (1979-) (orvos, biológus) Fuentes, Lucía Núnez, Vanessa Escolano, Amelia Redondo, Juan Miguel De Clerk, Nora Metzger, Daniel Valledor, Annabel F. Ricote, Mercedes
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DOI
Intézményi repozitóriumban (DEA) tárolt változat
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