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001-es BibID:	BIBFORM103144
035-os BibID:	(WOS)000302142900005 (Scopus)84857752421
Első szerző:	Menendez-Gutierrez, Maria Piedad
Cím:	Biology and therapeutic applications of peroxisome proliferator- activated receptors / Maria P. Menendez-Gutierrez, Tamas Roszer, Mercedes Ricote
Dátum:	2012
ISSN:	1568-0266
Megjegyzések:	Peroxisome proliferator-activated receptors (PPARs) are ligand dependent transcription factors. The three mammalian PPARs are key regulators of fatty acid and lipoprotein metabolism, glucose homeostasis, cellular proliferation/differentiation and the immune response. PPARs are therefore important targets in the treatment of metabolic disorders such as insulin resistance and type 2 diabetes mellitus, and are also of interest in relation to chronic inflammatory diseases such as atherosclerosis, arthritis, chronic pulmonary inflammation, pancreatitis, inflammatory bowel disease, and psoriasis. Recent advances have attributed novel functions to PPARs in blood pressure regulation, neuroinflammation, nerve-cell protection, inflammatory pain reduction, and the hypothalamic control of metabolism. The abundant pleiotropic actions of PPARs suggest that PPAR agonists have enormous therapeutic potential. However, current PPAR-based therapies often have undesired side effects due to the concomitant activation of PPARs in non-target cells. There is therefore growing interest in the development of cell-specific PPAR agonists and improvement of the clinical use of PPAR ligands. This review gives an overview of PPAR functions and discusses the current and potential medical implications of PPAR ligands in various pathologies, ranging from metabolic disorders to cardiovascular disease, chronic inflammation, neurodegenerative disorders and cancer.
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk Nuclear receptors PPAR transcription metabolism inflammation cardiovascular disease neuroinflammation cancer
Megjelenés:	Current Topics In Medicinal Chemistry. - 12 : 6 (2012), p. 548-584. -
További szerzők:	Röszer Tamás (1979-) (orvos, biológus) Ricote, Mercedes
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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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
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM103155
035-os BibID:	(WOS)000285688700070 (Scopus)79251561239
Első szerző:	Röszer Tamás (orvos, biológus)
Cím:	Autoimmune kidney disease and impaired engulfment of apoptotic cells in mice with macrophage peroxisome proliferator-activated gamma or retinoid X receptor alpha deficiency / Tamás Rőszer, María P. Menéndez-Gutiérrez, Martina I. Lefterova, Daniel Alameda, Vanessa Núñez, Mitchell A. Lazar, Thierry Fischer, Mercedes Ricote
Dátum:	2011
ISSN:	0022-1767 1550-6606
Megjegyzések:	Autoimmune glomerulonephritis is a common manifestation of systemic lupus erythematosus (SLE). In this study, we show that mice lacking macrophage expression of the heterodimeric nuclear receptors PPAR gamma or RXR alpha develop glomerulonephritis and autoantibodies to nuclear Ags, resembling the nephritis seen in SLE. These mice show deficiencies in phagocytosis and clearance of apoptotic cells, and they are unable to acquire an anti-inflammatory phenotype upon feeding of apoptotic cells, which is critical for the maintenance of self-tolerance. These results demonstrate that stimulation of PPAR gamma and RXR alpha in macrophages facilitates apoptotic cell engulfment, and they provide a potential strategy to avoid autoimmunity against dying cells and to attenuate SLE.
Tárgyszavak:	Természettudományok Biológiai tudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk
Megjelenés:	Journal of Immunology. - 186 : 1 (2011), p. 621-631. -
További szerzők:	Menendez-Gutierrez, Maria Piedad Lefterova, Martina I. Alameda, Daniel Núnez, Vanessa Lazar, Mitchell A. Fischer, Thierry Ricote, Mercedes
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM103136
035-os BibID:	(Wos)000324784800005 (Scopus)84883205841
Első szerző:	Röszer Tamás (orvos, biológus)
Cím:	Retinoid X receptors in macrophage biology / Tamás Rőszer, María P. Menéndez-Gutiérrez, Marta Cedenilla, Mercedes Ricote
Dátum:	2013
ISSN:	1043-2760
Megjegyzések:	Retinoid X receptors (RXRs) form a distinct and unique subclass within the nuclear receptor (NR) superfamily of ligand-dependent transcription factors. RXRs regulate a plethora of genetic programs, including cell differentiation, the immune response, and lipid and glucose metabolism. Recent advances reveal that RXRs are important regulators of macrophages, key players in inflammatory and metabolic disorders. This review outlines the versatility of RXR action in the control of macrophage gene transcription through its heterodimerization with other NRs or through RXR homodimerization. We also highlight the potential of RXR-controlled transcriptional programs as targets for the treatment of pathologies associated with altered macrophage function, such as atherosclerosis, insulin resistance, autoimmunity, and neurodegeneration.
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk nuclear receptors gene transcription macrophage inflammation lipid metabolism
Megjelenés:	Trends In Endocrinology And Metabolism. - 24 : 9 (2013), p.460-468. -
További szerzők:	Menendez-Gutierrez, Maria Piedad Cedenilla, Marta Ricote, Mercedes
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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