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Your search keyword '"Martinez-Chantar, María L."' showing total 18 results
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18 results on '"Martinez-Chantar, María L."'

1. p63 controls metabolic activation of hepatic stellate cells and fibrosis via an HER2-ACC1 pathway

Author

Fondevila, Marcos F., Novoa, Eva, Gonzalez-Rellan, Maria J., Fernandez, Uxia, Heras, Violeta, Porteiro, Begoña, Parracho, Tamara, Dorta, Valentina, Riobello, Cristina, da Silva Lima, Natalia, Seoane, Samuel, Garcia-Vence, Maria, Chantada-Vazquez, Maria P., Bravo, Susana B., Senra, Ana, Leiva, Magdalena, Marcos, Miguel, Sabio, Guadalupe, Perez-Fernandez, Roman, Dieguez, Carlos, Prevot, Vincent, Schwaninger, Markus, Woodhoo, Ashwin, Martinez-Chantar, Maria L., Schwabe, Robert, Cubero, Francisco J., Varela-Rey, Marta, Crespo, Javier, Iruzubieta, Paula, and Nogueiras, Ruben

Published
2024
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2. Anti-miR-873-5p improves alcohol-related liver disease by enhancing hepatic deacetylation via SIRT1

Author

Rodríguez-Agudo, Rubén, González-Recio, Irene, Serrano-Maciá, Marina, Bravo, Miren, Petrov, Petar, Blaya, Delia, Herranz, Jose María, Mercado-Gómez, María, Rejano-Gordillo, Claudia María, Lachiondo-Ortega, Sofía, Gil-Pitarch, Clàudia, Azkargorta, Mikel, Van Liempd, Sebastiaan Martijn, Martinez-Cruz, Luis Alfonso, Simão, A.L., Elortza, Félix, Martín, César, Nevzorova, Yulia A., Cubero, Francisco Javier, Delgado, Teresa C., Argemi, Josepmaria, Bataller, Ramón, Schoonjans, Kristina, Banales, Jesús M., Castro, Rui E., Sancho-Bru, Pau, Avila, Matías A., Julve, Josep, Jover, Ramiro, Mabe, Jon, Simon, Jorge, Goikoetxea-Usandizaga, Naroa, and Martínez-Chantar, María L.

Published
2024
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3. Neddylation of phosphoenolpyruvate carboxykinase 1 controls glucose metabolism

Author

Gonzalez-Rellan, María J., Fernández, Uxía, Parracho, Tamara, Novoa, Eva, Fondevila, Marcos F., da Silva Lima, Natalia, Ramos, Lucía, Rodríguez, Amaia, Serrano-Maciá, Marina, Perez-Mejias, Gonzalo, Chantada-Vazquez, Pilar, Riobello, Cristina, Veyrat-Durebex, Christelle, Tovar, Sulay, Coppari, Roberto, Woodhoo, Ashwin, Schwaninger, Markus, Prevot, Vincent, Delgado, Teresa C., Lopez, Miguel, Diaz-Quintana, Antonio, Dieguez, Carlos, Guallar, Diana, Frühbeck, Gema, Diaz-Moreno, Irene, Bravo, Susana B., Martinez-Chantar, Maria L., and Nogueiras, Ruben

Published
2023
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4. Hepatocyte-specific O-GlcNAc transferase downregulation ameliorates nonalcoholic steatohepatitis by improving mitochondrial function

Author

Gonzalez-Rellan, Maria J., Parracho, Tamara, Heras, Violeta, Rodriguez, Amaia, Fondevila, Marcos F., Novoa, Eva, Lima, Natalia, Varela-Rey, Marta, Senra, Ana, Chantada-Vazquez, Maria D.P., Ameneiro, Cristina, Bernardo, Ganeko, Fernandez-Ramos, David, Lopitz-Otsoa, Fernando, Bilbao, Jon, Guallar, Diana, Fidalgo, Miguel, Bravo, Susana, Dieguez, Carlos, Martinez-Chantar, Maria L., Millet, Oscar, Mato, Jose M., Schwaninger, Markus, Prevot, Vincent, Crespo, Javier, Frühbeck, Gema, Iruzubieta, Paula, and Nogueiras, Ruben

Published
2023
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5. miR-873-5p targets mitochondrial GNMT-Complex II interface contributing to non-alcoholic fatty liver disease

Author

Fernández-Tussy, Pablo, Fernández-Ramos, David, Lopitz-Otsoa, Fernando, Simón, Jorge, Barbier-Torres, Lucía, Gomez-Santos, Beatriz, Nuñez-Garcia, Maitane, Azkargorta, Mikel, Gutiérrez-de Juan, Virginia, Serrano-Macia, Marina, Rodríguez-Agudo, Rubén, Iruzubieta, Paula, Anguita, Juan, Castro, Rui E., Champagne, Devin, Rincón, Mercedes, Elortza, Felix, Arslanow, Anita, Krawczyk, Marcin, Lammert, Frank, Kirchmeyer, Mélanie, Behrmann, Iris, Crespo, Javier, Lu, Shelly C., Mato, José M., Varela-Rey, Marta, Aspichueta, Patricia, Delgado, Teresa C., and Martínez-Chantar, María L.

Published
2019
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6. Involvement of G protein-coupled receptor kinase 2 (GRK2) in the development of non-alcoholic steatosis and steatohepatitis in mice and humans

Author

Cruces-Sande, Marta, Vila-Bedmar, Rocío, Arcones, Alba C., González-Rodríguez, Águeda, Rada, Patricia, Gutiérrez-de-Juan, Virginia, Vargas-Castrillón, Javier, Iruzubieta, Paula, Sánchez-González, Cristina, Formentini, Laura, Crespo, Javier, García-Monzón, Carmelo, Martínez-Chantar, María L., Valverde, Ángela M., Mayor, Federico, Jr, and Murga, Cristina

Published
2018
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8. Mitochondrial dysfunction-associated microbiota establishes a transmissible refractory response to anti-TNF therapy during ulcerative colitis.

Author

Peña-Cearra, Ainize, Castelo, Janire, Lavín, Jose Luis, Gonzalez-Lopez, Monika, Pascual-Itoiz, Miguel Angel, Fuertes, Miguel, Gutiérrez de Juan, Virginia, Bárcena, Laura, Martín-Ruiz, Itziar, Pellón, Aize, Seoane, Iratxe, Barriales, Diego, Palacios, Ainhoa, Fullaondo, Asier, Rodríguez-Lago, Iago, Martinez-Chantar, María L., Aransay, Ana Mª, Rodriguez, Hector, Anguita, Juan, and Abecia, Leticia

Published
2023
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11. Hepatoma Cells From Mice Deficient in Glycine N-Methyltransferase Have Increased RAS Signaling and Activation of Liver Kinase B1

Author

Martínez–López, Nuria, García–Rodríguez, Juan L., Varela–Rey, Marta, Gutiérrez, Virginia, Fernández–Ramos, David, Beraza, Naiara, Aransay, Ana M., Schlangen, Karin, Lozano, Juan Jose, Aspichueta, Patricia, Luka, Zigmund, Wagner, Conrad, Evert, Matthias, Calvisi, Diego F., Lu, Shelly C., Mato, José M., and Martínez–Chantar, María L.

Published
2012
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15. Liver osteopontin is required to prevent the progression of age‐related nonalcoholic fatty liver disease.

Author

Gómez‐Santos, Beatriz, Saenz de Urturi, Diego, Nuñez‐García, Maitane, Gonzalez‐Romero, Francisco, Buque, Xabier, Aurrekoetxea, Igor, Gutiérrez de Juan, Virginia, Gonzalez‐Rellan, Maria J., García‐Monzón, Carmelo, González‐Rodríguez, Águeda, Mosteiro, Lorena, Errazti, Gaizka, Mifsut, Patricia, Gaztambide, Sonia, Castaño, Luis, Martin, Cesar, Nogueiras, Rubén, Martinez‐Chantar, María L., Syn, Wing‐Kin, and Aspichueta, Patricia

Subjects
FATTY liver, OSTEOPONTIN, ANIMAL models for aging, LIVER, LIPID metabolism, P53 antioncogene, LIVER cells
Abstract

Osteopontin (OPN), a senescence‐associated secretory phenotype factor, is increased in patients with nonalcoholic fatty liver disease (NAFLD). Cellular senescence has been associated with age‐dependent hepatosteatosis. Thus, we investigated the role of OPN in the age‐related hepatosteatosis. For this, human serum samples, animal models of aging, and cell lines in which senescence was induced were used. Metabolic fluxes, lipid, and protein concentration were determined. Among individuals with a normal liver, we observed a positive correlation between serum OPN levels and increasing age. This correlation with age, however, was absent in patients with NAFLD. In wild‐type (WT) mice, serum and liver OPN were increased at 10 months old (m) along with liver p53 levels and remained elevated at 20m. Markers of liver senescence increased in association with synthesis and concentration of triglycerides (TG) in 10m OPN‐deficient (KO) hepatocytes when compared to WT hepatocytes. These changes in senescence and lipid metabolism in 10m OPN‐KO mice liver were associated with the decrease of 78 kDa glucose‐regulated protein (GRP78), induction of ER stress, and the increase in fatty acid synthase and CD36 levels. OPN deficiency in senescent cells also diminished GRP78, the accumulation of intracellular TG, and the increase in CD36 levels. In 20m mice, OPN loss led to increased liver fibrosis. Finally, we showed that OPN expression in vitro and in vivo was regulated by p53. In conclusion, OPN deficiency leads to earlier cellular senescence, ER stress, and TG accumulation during aging. The p53‐OPN axis is required to inhibit the onset of age‐related hepatosteatosis. [ABSTRACT FROM AUTHOR]

Published
2020
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18. Schwann cell autophagy, myelinophagy, initiates myelin clearance from injured nerves.

Author

Gomez-Sanchez, Jose A., Carty, Lucy, Iruarrizaga-Lejarreta, Marta, Palomo-Irigoyen, Marta, Varela-Rey, Marta, Griffith, Megan, Hantke, Janina, Macias-Camara, Nuria, Azkargorta, Mikel, Aurrekoetxea, Igor, De Juan, Virginia Gutiérrez, Jefferies, Harold B. J., Aspichueta, Patricia, Elortza, Félix, Aransay, Ana M., Martinez-Chantar, María L., Baas, Frank, Mato, José M., Mirsky, Rhona, and Woodhoo, Ashwin

Subjects
*SCHWANN cells, *AUTOPHAGY, *MYELIN, *PERIPHERAL nervous system, *CYTOLOGICAL research
Abstract

Although Schwann cell myelin breakdown is the universal outcome of a remarkably wide range of conditions that cause disease or injury to peripheral nerves, the cellular and molecular mechanisms that make Schwann cell-mediated myelin digestion possible have not been established. We report that Schwann cells degrade myelin after injury by a novel form of selective autophagy, myelinophagy. Autophagy was up-regulated by myelinating Schwann cells after nerve injury, myelin debris was present in autophagosomes, and pharmacological and genetic inhibition of autophagy impaired myelin clearance. Myelinophagy was positively regulated by the Schwann cell JNK/c-Jun pathway, a central regulator of the Schwann cell reprogramming induced by nerve injury. We also present evidence that myelinophagy is defective in the injured central nervous system. These results reveal an important role for inductive autophagy during Wallerian degeneration, and point to potential mechanistic targets for accelerating myelin clearance and improving demyelinating disease. [ABSTRACT FROM AUTHOR]

Published
2015
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