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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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2.

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
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Intézményi repozitóriumban (DEA) tárolt változat
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3.

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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Intézményi repozitóriumban (DEA) tárolt változat
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4.

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
OTKA
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
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5.

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
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Intézményi repozitóriumban (DEA) tárolt változat
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6.

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
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Intézményi repozitóriumban (DEA) tárolt változat
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7.

001-es BibID:BIBFORM103067
035-os BibID:(cikkazonosító)698730 (WOS)000283426500001 (Scopus)77954589084
Első szerző:Röszer Tamás (orvos, biológus)
Cím:PPARs in the renal regulation of systemic blood pressure / Tamás Röszer, Mercedes Ricote
Dátum:2010
ISSN:1687-4757 1687-4765
Megjegyzések:Recent research has revealed roles for the peroxisome proliferator activated receptor (PPAR) family of transcription factors in blood pressure regulation, expanding the possible therapeutic use of PPAR ligands. PPAR and PPAR modulate the renin-angiotensin-aldosterone system (RAAS), a major regulator of systemic blood pressure and interstitial fluid volume by transcriptional control of renin, angiotensinogen, angiotensin converting enzyme (ACE) and angiotensin II receptor 1 (AT-R1). Blockade of RAAS is an important therapeutic target in hypertension management and attenuates microvascular damage, glomerular inflammation and left ventricular hypertrophy in hypertensive patients and also show antidiabetic effects. The mechanisms underlying the benefits of RAAS inhibition appear to involve PPAR-regulated pathways. This review summarizes current knowledge on the role of PPARs in the transcriptional control of the RAAS and the possible use of PPAR ligands in the treatment of RAAS dependent hypertension.
Tárgyszavak:Természettudományok Biológiai tudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:PPAR Research. - 2010 (2010), p. 1-11. -
További szerzők:Ricote, Mercedes
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Intézményi repozitóriumban (DEA) tárolt változat
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