16 results on '"A. Colio"'
Search Results
2. N-Terminal Pro-Brain Natriuretic Peptide Is Associated with a Future Diagnosis of Cancer in Patients with Coronary Artery Disease.
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José Tuñón, Javier Higueras, Nieves Tarín, Carmen Cristóbal, Óscar Lorenzo, Luis Blanco-Colio, José Luis Martín-Ventura, Ana Huelmos, Joaquín Alonso, Álvaro Aceña, Ana Pello, Rocío Carda, Dolores Asensio, Ignacio Mahíllo-Fernández, Lorenzo López Bescós, Jesús Egido, and Jerónimo Farré
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Medicine ,Science - Abstract
Several papers have reported elevated plasma levels of natriuretic peptides in patients with a previous diagnosis of cancer. We have explored whether N-terminal pro-brain natriuretic peptide (NT-proBNP) plasma levels predict a future diagnosis of cancer in patients with coronary artery disease (CAD).We studied 699 patients with CAD free of cancer. At baseline, NT-proBNP, galectin-3, monocyte chemoattractant protein-1, soluble tumor necrosis factor-like weak inducer of apoptosis, high-sensitivity C-reactive protein, and high-sensitivity cardiac troponin I plasma levels were assessed. The primary outcome was new cancer diagnosis. The secondary outcome was cancer diagnosis, heart failure requiring hospitalization, or death.After 2.15±0.98 years of follow-up, 24 patients developed cancer. They were older (68.5 [61.5, 75.8] vs 60.0 [52.0, 72.0] years; p=0.011), had higher NT-proBNP (302.0 [134.8, 919.8] vs 165.5 [87.4, 407.5] pg/ml; p=0.040) and high-sensitivity C-reactive protein (3.27 [1.33, 5.94] vs 1.92 [0.83, 4.00] mg/L; p=0.030), and lower triglyceride (92.5 [70.5, 132.8] vs 112.0 [82.0, 157.0] mg/dl; p=0.044) plasma levels than those without cancer. NT-proBNP (Hazard Ratio [HR]=1.030; 95% Confidence Interval [CI]=1.008-1.053; p=0.007) and triglyceride levels (HR=0.987; 95%CI=0.975-0.998; p=0.024) were independent predictors of a new cancer diagnosis (multivariate Cox regression analysis). When patients in whom the suspicion of cancer appeared in the first one-hundred days after blood extraction were excluded, NT-proBNP was the only predictor of cancer (HR=1.061; 95%CI=1.034-1.088; p
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- 2015
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3. Reduced sTWEAK and increased sCD163 levels in HIV-infected patients: modulation by antiretroviral treatment, HIV replication and HCV co-infection.
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Luis M Beltrán, Rocío Muñoz Hernández, Rebeca S de Pablo Bernal, José S García Morillo, Jesús Egido, Manuel Leal Noval, Sara Ferrando-Martinez, Luis M Blanco-Colio, Miguel Genebat, José R Villar, Rafael Moreno-Luna, and Juan Antonio Moreno
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Medicine ,Science - Abstract
Patients infected with the human immunodeficiency virus (HIV) have an increased risk of cardiovascular disease due to increased inflammation and persistent immune activation. CD163 is a macrophage scavenger receptor that is involved in monocyte-macrophage activation in HIV-infected patients. CD163 interacts with TWEAK, a member of the TNF superfamily. Circulating levels of sTWEAK and sCD163 have been previously associated with cardiovascular disease, but no previous studies have fully analyzed their association with HIV.The aim of this study was to analyze circulating levels of sTWEAK and sCD163 as well as other known markers of inflammation (hsCRP, IL-6 and sTNFRII) and endothelial dysfunction (sVCAM-1 and ADMA) in 26 patients with HIV before and after 48 weeks of antiretroviral treatment (ART) and 23 healthy subjects.Patients with HIV had reduced sTWEAK levels and increased sCD163, sVCAM-1, ADMA, hsCRP, IL-6 and sTNFRII plasma concentrations, as well as increased sCD163/sTWEAK ratio, compared with healthy subjects. Antiretroviral treatment significantly reduced the concentrations of sCD163, sVCAM-1, hsCRP and sTNFRII, although they remained elevated when compared with healthy subjects. Antiretroviral treatment had no effect on the concentrations of ADMA and sTWEAK, biomarkers associated with endothelial function. The use of protease inhibitors as part of antiretroviral therapy and the presence of HCV-HIV co-infection and/or active HIV replication attenuated the ART-mediated decrease in sCD163 plasma concentrations.HIV-infected patients showed a proatherogenic profile characterized by increased inflammatory, immune-activation and endothelial-dysfunction biomarkers that partially improved after ART. HCV-HIV co-infection and/or active HIV replication enhanced immune activation despite ART.
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- 2014
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4. TWEAK promotes peritoneal inflammation.
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Ana Belen Sanz, Luiz Stark Aroeira, Teresa Bellon, Gloria del Peso, Jose Jimenez-Heffernan, Beatriz Santamaria, Maria Dolores Sanchez-Niño, Luis Miguel Blanco-Colio, Manuel Lopez-Cabrera, Marta Ruiz-Ortega, Jesus Egido, Rafael Selgas, and Alberto Ortiz
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Medicine ,Science - Abstract
Peritoneal dialysis (PD) is complicated by peritonitis episodes that cause loss of mesothelium and eventually sclerosing peritonitis. An improved understanding of the molecular contributors to peritoneal injury and defense may increase the therapeutic armamentarium to optimize peritoneal defenses while minimizing peritoneal injury. There is no information on the expression and function of the cytokine TWEAK and its receptor Fn14 during peritoneal injury. Fn14 expression and soluble TWEAK levels were measured in human PD peritoneal effluent cells or fluids with or without peritonitis. Fn14 expression was also analyzed in peritoneal biopsies from PD patients. Actions of intraperitoneal TWEAK were studied in mice in vivo. sTWEAK levels were increased in peritoneal effluent in PD peritonitis. Effluent sTWEAK levels correlated with the number of peritoneal macrophages (r=0.491, p=0.002). Potential TWEAK targets that express the receptor Fn14 include mesothelial cells and macrophages, as demonstrated by flow cytometry of peritoneal effluents and by analysis of peritoneal biopsies. Peritoneal biopsy Fn14 correlated with mesothelial injury, fibrosis and inflammation, suggesting a potential deleterious effect of TWEAK/Fn14. In this regard, intraperitoneal TWEAK administration to mice promoted peritoneal inflammation characterized by increased peritoneal effluent MCP-1, Fn14 and Gr1+ macrophages, increased mesothelial Fn14, MCP-1 and CCL21 expression and submesothelial tissue macrophage recruitment. Taken together these data suggest that the TWEAK/Fn14 system may promote inflammation and tissue injury during peritonitis and PD.
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- 2014
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5. Hyperlipidemia-associated renal damage decreases Klotho expression in kidneys from ApoE knockout mice.
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Cristina Sastre, Alfonso Rubio-Navarro, Irene Buendía, Carmen Gómez-Guerrero, Julia Blanco, Sebastian Mas, Jesús Egido, Luis Miguel Blanco-Colio, Alberto Ortiz, and Juan Antonio Moreno
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Medicine ,Science - Abstract
BackgroundKlotho is a renal protein with anti-aging properties that is downregulated in conditions related to kidney injury. Hyperlipidemia accelerates the progression of renal damage, but the mechanisms of the deleterious effects of hyperlipidemia remain unclear.MethodsWe evaluated whether hyperlipidemia modulates Klotho expression in kidneys from C57BL/6 and hyperlipidemic apolipoprotein E knockout (ApoE KO) mice fed with a normal chow diet (ND) or a Western-type high cholesterol-fat diet (HC) for 5 to 10 weeks, respectively.ResultsIn ApoE KO mice, the HC diet increased serum and renal cholesterol levels, kidney injury severity, kidney macrophage infiltration and inflammatory chemokine expression. A significant reduction in Klotho mRNA and protein expression was observed in kidneys from hypercholesteromic ApoE KO mice fed a HC diet as compared with controls, both at 5 and 10 weeks. In order to study the mechanism involved in Klotho down-regulation, murine tubular epithelial cells were treated with ox-LDL. Oxidized-LDL were effectively uptaken by tubular cells and decreased both Klotho mRNA and protein expression in a time- and dose-dependent manner in these cells. Finally, NF-κB and ERK inhibitors prevented ox-LDL-induced Klotho downregulation.ConclusionOur results suggest that hyperlipidemia-associated kidney injury decreases renal expression of Klotho. Therefore, Klotho could be a key element explaining the relationship between hyperlipidemia and aging with renal disease.
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- 2013
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6. TWEAK activates the non-canonical NFkappaB pathway in murine renal tubular cells: modulation of CCL21.
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Ana B Sanz, Maria D Sanchez-Niño, Maria C Izquierdo, Aniela Jakubowski, Pilar Justo, Luis M Blanco-Colio, Marta Ruiz-Ortega, Rafael Selgas, Jesús Egido, and Alberto Ortiz
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Medicine ,Science - Abstract
TWEAK is a member of the TNF superfamily of cytokines that contribute to kidney tubulointerstitial injury. It has previously been reported that TWEAK induces transient nuclear translocation of RelA and expression of RelA-dependent cytokines in renal tubular cells. Additionally, TWEAK induced long-lasting NFkappaB activation suggestive of engagement of the non-canonical NFkappaB pathway. We now explore TWEAK-induced activation of NFkappaB2 and RelB, as well as expression of CCL21, a T-cell chemotactic factor, in cultured murine tubular epithelial cells and in healthy kidneys in vivo. In cultured tubular cells, TWEAK and TNFalpha activated different DNA-binding NFkappaB complexes. TWEAK-induced sustained NFkappaB activation was associated with NFkappaB2 p100 processing to p52 via proteasome and nuclear translocation and DNA-binding of p52 and RelB. TWEAK, but not TNFalpha used as control), induced a delayed increase in CCL21a mRNA (3.5+/-1.22-fold over control) and CCL21 protein (2.5+/-0.8-fold over control), which was prevented by inhibition of the proteasome, or siRNA targeting of NIK or RelB, but not by RelA inhibition with parthenolide. A second NFkappaB2-dependent chemokine, CCL19, was upregulates by TWEAK, but not by TNFalpha. However, both cytokines promoted chemokine RANTES expression (3-fold mRNA at 24 h). In vivo, TWEAK induced nuclear NFkappaB2 and RelB translocation and CCL21a mRNA (1.5+/-0.3-fold over control) and CCL21 protein (1.6+/-0.5-fold over control) expression in normal kidney. Increased tubular nuclear RelB and tubular CCL21 expression in acute kidney injury were decreased by neutralization (2+/-0.9 vs 1.3+/-0.6-fold over healthy control) or deficiency of TWEAK (2+/-0.9 vs 0.8+/-0.6-fold over healthy control). Moreover, anti-TWEAK treatment prevented the recruitment of T cells to the kidney in this model (4.1+/-1.4 vs 1.8+/-1-fold over healthy control). Our results thus identify TWEAK as a regulator of non-canonical NFkappaB activation and CCL21 expression in tubular cells thus promoting lymphocyte recruitment to the kidney during acute injury.
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- 2010
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7. Essential role of TGF-beta/Smad pathway on statin dependent vascular smooth muscle cell regulation.
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Juan Rodríguez-Vita, Eva Sánchez-Galán, Beatriz Santamaría, Elsa Sánchez-López, Raquel Rodrigues-Díez, Luís Miguel Blanco-Colio, Jesús Egido, Alberto Ortiz, and Marta Ruiz-Ortega
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Medicine ,Science - Abstract
BackgroundThe 3-hydroxy-3-methylglutaryl CoA reductase inhibitors (also called statins) exert proven beneficial effects on cardiovascular diseases. Recent data suggest a protective role for Transforming Growth Factor-beta (TGF-beta) in atherosclerosis by regulating the balance between inflammation and extracellular matrix accumulation. However, there are no studies about the effect of statins on TGF-beta/Smad pathway in atherosclerosis and vascular cells.MethodologyIn cultured vascular smooth muscle cells (VSMCs) statins enhanced Smad pathway activation caused by TGF-beta. In addition, statins upregulated TGF-beta receptor type II (TRII), and increased TGF-beta synthesis and TGF-beta/Smad-dependent actions. In this sense, statins, through Smad activation, render VSMCs more susceptible to TGF-beta induced apoptosis and increased TGF-beta-mediated ECM production. It is well documented that high doses of statins induce apoptosis in cultured VSMC in the presence of serum; however the precise mechanism of this effect remains to be elucidated. We have found that statins-induced apoptosis was mediated by TGF-beta/Smad pathway. Finally, we have described that RhoA inhibition is a common intracellular mechanisms involved in statins effects. The in vivo relevance of these findings was assessed in an experimental model of atherosclerosis in apolipoprotein E deficient mice: Treatment with Atorvastatin increased Smad3 phosphorylation and TRII overexpression, associated to elevated ECM deposition in the VSMCs within atheroma plaques, while apoptosis was not detected.ConclusionsStatins enhance TGF-beta/Smad pathway, regulating ligand levels, receptor, main signaling pathway and cellular responses of VSMC, including apoptosis and ECM accumulation. Our findings show that TGF-beta/Smad pathway is essential for statins-dependent actions in VSMCs.
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- 2008
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8. N-Terminal Pro-Brain Natriuretic Peptide Is Associated with a Future Diagnosis of Cancer in Patients with Coronary Artery Disease
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Óscar Lorenzo, Ignacio Mahillo-Fernández, Álvaro Aceña, Jesús Egido, Nieves Tarín, José Tuñón, Ana Huelmos, Dolores Asensio, Lorenzo López Bescós, José Luis Martín-Ventura, Joaquín Alonso, Rocío Carda, Javier Higueras, Carmen Cristóbal, Ana Maria Pello, Jerónimo Farré, Luis Miguel Blanco-Colio, UAM. Departamento de Medicina, and Instituto de Investigación Sanitaria Fundación Jiménez Díaz (IIS-FJD)
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Male ,medicine.medical_specialty ,Medicina ,medicine.drug_class ,Galectin 3 ,lcsh:Medicine ,Coronary Artery Disease ,Coronary artery disease ,Gastroenterology ,Atrial natriuretic peptide ,Risk Factors ,Internal medicine ,Neoplasms ,Troponin I ,Natriuretic Peptide, Brain ,Natriuretic peptide ,Medicine ,Humans ,cardiovascular diseases ,Natriuretic peptides ,lcsh:Science ,Triglycerides ,Cancer ,Aged ,Proportional Hazards Models ,Heart Failure ,Multidisciplinary ,biology ,business.industry ,lcsh:R ,C-reactive protein ,Middle Aged ,medicine.disease ,Peptide Fragments ,C-Reactive Protein ,Galectin-3 ,Heart failure ,Cardiology ,biology.protein ,Linear Models ,lcsh:Q ,Female ,business ,Biomarkers ,Follow-Up Studies ,Research Article - Abstract
Objective Several papers have reported elevated plasma levels of natriuretic peptides in patients with a previous diagnosis of cancer. We have explored whether N-terminal pro-brain natriuretic peptide (NT-proBNP) plasma levels predict a future diagnosis of cancer in patients with coronary artery disease (CAD). Methods We studied 699 patients with CAD free of cancer. At baseline, NT-proBNP, galectin-3, monocyte chemoattractant protein-1, soluble tumor necrosis factor-like weak inducer of apoptosis, high-sensitivity C-reactive protein, and high-sensitivity cardiac troponin I plasma levels were assessed. The primary outcome was new cancer diagnosis. The secondary outcome was cancer diagnosis, heart failure requiring hospitalization, or death. Results After 2.15±0.98 years of follow-up, 24 patients developed cancer. They were older (68.5 [61.5, 75.8] vs 60.0 [52.0, 72.0] years; p=0.011), had higher NT-proBNP (302.0 [134.8, 919.8] vs 165.5 [87.4, 407.5] pg/ml; p=0.040) and high-sensitivity C-reactive protein (3.27 [1.33, 5.94] vs 1.92 [0.83, 4.00] mg/L; p=0.030), and lower triglyceride (92.5 [70.5, 132.8] vs 112.0 [82.0, 157.0] mg/dl; p=0.044) plasma levels than those without cancer. NT-proBNP (Hazard Ratio [HR]=1.030; 95% Confidence Interval [CI]=1.008-1.053; p=0.007) and triglyceride levels (HR=0.987; 95%CI=0.975-0.998; p=0.024) were independent predictors of a new cancer diagnosis (multivariate Cox regression analysis). When patients in whom the suspicion of cancer appeared in the first one-hundred days after blood extraction were excluded, NT-proBNP was the only predictor of cancer (HR=1.061; 95% CI=1.034-1.088; p, This work was supported by grants from Fondo de Investigaciones Sanitarias (PI05/0451, PI05/1497,PI05/2475, PI05/1043, PS09/01405, PI10/ 00072, and PI10/0234, PI14/1567, Programa de Estabilización to LBC); Spanish Society of Cardiology and Spanish Heart Foundation; Spanish Society of Arteriosclerosis; RECAVA (RD06/0014/0035, www. recava.com); Fundación Lilly; and Instituto de Salud Carlos III FEDER (FJD biobank: RD09/0076/00101).
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- 2014
9. Plasma Levels of Monocyte Chemoattractant Protein-1, n-Terminal Fragment of Brain Natriuretic Peptide and Calcidiol Are Independently Associated with the Complexity of Coronary Artery Disease
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Martín-Reyes, Roberto, primary, Franco-Peláez, Juan Antonio, additional, Lorenzo, Óscar, additional, González-Casaus, María Luisa, additional, Pello, Ana María, additional, Aceña, Álvaro, additional, Carda, Rocío, additional, Martín-Ventura, José Luis, additional, Blanco-Colio, Luis, additional, Martín-Mariscal, María Luisa, additional, Martínez-Milla, Juan, additional, Villa-Bellosta, Ricardo, additional, Piñero, Antonio, additional, Navarro, Felipe, additional, Egido, Jesús, additional, and Tuñón, José, additional
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- 2016
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10. Hyperlipidemia-associated renal damage decreases Klotho expression in kidneys from ApoE knockout mice
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Jesús Egido, Carmen Gomez-Guerrero, Luis Miguel Blanco-Colio, Julia Blanco, Cristina Sastre, Alberto Ortiz, Irene Buendía, Juan Antonio Moreno, Sebastian Mas, Alfonso Rubio-Navarro, and UAM. Departamento de Medicina
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Apolipoprotein E ,Male ,Anatomy and Physiology ,Animal Nutrition ,Mouse ,Gene Expression ,Epithelial cells ,Bioinformatics ,urologic and male genital diseases ,Kidney ,Mice ,Hyperlipidemia ,Chronic Kidney Disease ,Klotho ,Cells, Cultured ,Glucuronidase ,Animal Management ,Mice, Knockout ,Multidisciplinary ,Renal damage ,Agriculture ,Animal Models ,female genital diseases and pregnancy complications ,Lipoproteins, LDL ,Cholesterol ,Nephrology ,Knockout mouse ,Cytokines ,Medicine ,Christian ministry ,Kidney Diseases ,Inflammation Mediators ,Research Article ,medicine.medical_specialty ,Medicina ,Science ,Hyperlipidemias ,Cell Line ,Molecular Genetics ,Apolipoproteins E ,Model Organisms ,medicine ,Genetics ,Animals ,Klotho Proteins ,Biology ,Gynecology ,Inflammation ,Renal Physiology ,business.industry ,Computational Biology ,Kidneys ,Renal System ,medicine.disease ,Lipid Metabolism ,Diet ,Disease Models, Animal ,Oxidative Stress ,Gene Expression Regulation ,Oxidative stress ,Tubulointerstitial Disease ,Protein expression ,Veterinary Science ,business - Abstract
Background: Klotho is a renal protein with anti-aging properties that is downregulated in conditions related to kidney injury. Hyperlipidemia accelerates the progression of renal damage, but the mechanisms of the deleterious effects of hyperlipidemia remain unclear. Methods: We evaluated whether hyperlipidemia modulates Klotho expression in kidneys from C57BL/6 and hyperlipidemic apolipoprotein E knockout (ApoE KO) mice fed with a normal chow diet (ND) or a Western-type high cholesterol-fat diet (HC) for 5 to 10 weeks, respectively. Results: In ApoE KO mice, the HC diet increased serum and renal cholesterol levels, kidney injury severity, kidney macrophage infiltration and inflammatory chemokine expression. A significant reduction in Klotho mRNA and protein expression was observed in kidneys from hypercholesteromic ApoE KO mice fed a HC diet as compared with controls, both at 5 and 10 weeks. In order to study the mechanism involved in Klotho down-regulation, murine tubular epithelial cells were treated with ox-LDL. Oxidized-LDL were effectively uptaken by tubular cells and decreased both Klotho mRNA and protein expression in a time- and dose-dependent manner in these cells. Finally, NF-κB and ERK inhibitors prevented ox-LDL-induced Klotho downregulation. Conclusion: Our results suggest that hyperlipidemia-associated kidney injury decreases renal expression of Klotho. Therefore, Klotho could be a key element explaining the relationship between hyperlipidemia and aging with renal disease., This work has been supported by grants from FIS (Programa Miguel Servet: CP10/00479) to JAM and ISCIII (Programa de Estabilizacio´n) and PI10/00234 to LMBC. Fundacio´n Conchita Ra´bago to CS and ARN. Ministry of Science (SAF2012/38830) and Sociedad Espan˜ola de Nefrologia to CGG. ISCIII and FEDER funds PS09/00447, Sociedad Espan˜ola de Nefrologia, ISCIII-RETIC REDinREN/RD06/0016, Comunidad de Madrid/CIFRA/S2010/BMD-2378 to AO, and ISCIII-Redes RECAVA (RD06/0014/0035) REDINREN (RD12/0021/), European Network (HEALTH F2-2008-200647), Euro Salud EUS2005-03565, cvREMOD, Fundacion Lilly, FRIAT and ISCIII fund PI10/00072 to JE. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
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- 2013
11. N-Terminal Pro-Brain Natriuretic Peptide Is Associated with a Future Diagnosis of Cancer in Patients with Coronary Artery Disease
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Tuñón, José, primary, Higueras, Javier, additional, Tarín, Nieves, additional, Cristóbal, Carmen, additional, Lorenzo, Óscar, additional, Blanco-Colio, Luis, additional, Martín-Ventura, José Luis, additional, Huelmos, Ana, additional, Alonso, Joaquín, additional, Aceña, Álvaro, additional, Pello, Ana, additional, Carda, Rocío, additional, Asensio, Dolores, additional, Mahíllo-Fernández, Ignacio, additional, López Bescós, Lorenzo, additional, Egido, Jesús, additional, and Farré, Jerónimo, additional
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- 2015
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12. TWEAK Promotes Peritoneal Inflammation
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Sanz, Ana Belen, primary, Aroeira, Luiz Stark, additional, Bellon, Teresa, additional, del Peso, Gloria, additional, Jimenez-Heffernan, Jose, additional, Santamaria, Beatriz, additional, Sanchez-Niño, Maria Dolores, additional, Blanco-Colio, Luis Miguel, additional, Lopez-Cabrera, Manuel, additional, Ruiz-Ortega, Marta, additional, Egido, Jesus, additional, Selgas, Rafael, additional, and Ortiz, Alberto, additional
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- 2014
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13. Reduced sTWEAK and Increased sCD163 Levels in HIV-Infected Patients: Modulation by Antiretroviral Treatment, HIV Replication and HCV Co-Infection
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Beltrán, Luis M., primary, Muñoz Hernández, Rocío, additional, de Pablo Bernal, Rebeca S., additional, García Morillo, José S., additional, Egido, Jesús, additional, Noval, Manuel Leal, additional, Ferrando-Martinez, Sara, additional, Blanco-Colio, Luis M., additional, Genebat, Miguel, additional, Villar, José R., additional, Moreno-Luna, Rafael, additional, and Moreno, Juan Antonio, additional
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- 2014
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14. Hyperlipidemia-Associated Renal Damage Decreases Klotho Expression in Kidneys from ApoE Knockout Mice
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Sastre, Cristina, primary, Rubio-Navarro, Alfonso, additional, Buendía, Irene, additional, Gómez-Guerrero, Carmen, additional, Blanco, Julia, additional, Mas, Sebastian, additional, Egido, Jesús, additional, Blanco-Colio, Luis Miguel, additional, Ortiz, Alberto, additional, and Moreno, Juan Antonio, additional
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- 2013
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15. TWEAK Activates the Non-Canonical NFκB Pathway in Murine Renal Tubular Cells: Modulation of CCL21
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Sanz, Ana B., primary, Sanchez-Niño, Maria D., additional, Izquierdo, Maria C., additional, Jakubowski, Aniela, additional, Justo, Pilar, additional, Blanco-Colio, Luis M., additional, Ruiz-Ortega, Marta, additional, Selgas, Rafael, additional, Egido, Jesús, additional, and Ortiz, Alberto, additional
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- 2010
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16. Essential Role of TGF-β/Smad Pathway on Statin Dependent Vascular Smooth Muscle Cell Regulation
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Rodríguez-Vita, Juan, primary, Sánchez-Galán, Eva, additional, Santamaría, Beatriz, additional, Sánchez-López, Elsa, additional, Rodrigues-Díez, Raquel, additional, Blanco-Colio, Luís Miguel, additional, Egido, Jesús, additional, Ortiz, Alberto, additional, and Ruiz-Ortega, Marta, additional
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- 2008
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