Publicaciones en las que colabora con José Carlos Martínez Salgado (42)

2022

  1. Endothelial Activin Receptor-Like Kinase 1 (ALK1) Regulates Myofibroblast Emergence and Peritubular Capillary Stability in the Early Stages of Kidney Fibrosis

    Frontiers in Pharmacology, Vol. 13

2021

  1. Dissecting the Involvement of Ras GTPases in Kidney Fibrosis

    Genes, Vol. 12, Núm. 6

2020

  1. Impaired Tubular Reabsorption Is the Main Mechanism Explaining Increases in Urinary NGAL Excretion Following Acute Kidney Injury in Rats

    Toxicological sciences : an official journal of the Society of Toxicology, Vol. 175, Núm. 1, pp. 75-86

  2. Pathophysiological mechanisms underlying a rat model of triple whammy acute kidney injury

    Laboratory Investigation, Vol. 100, Núm. 11, pp. 1455-1464

2019

  1. Cardiotrophin-1 opposes renal fibrosis in mice: Potential prevention of chronic kidney disease

    Acta Physiologica, Vol. 226, Núm. 2

2016

  1. Absence of K-Ras Reduces Proliferation and Migration But Increases Extracellular Matrix Synthesis in Fibroblasts

    Journal of Cellular Physiology, Vol. 231, Núm. 10, pp. 2224-2235

  2. Identification of bone morphogenetic protein 9 (BMP9) as a novel profibrotic factor in vitro

    Cellular Signalling, Vol. 28, Núm. 9, pp. 1252-1261

  3. Mechanisms of triple whammy acute kidney injury

    Pharmacology and Therapeutics, Vol. 167, pp. 132-145

2015

  1. Acute tubular necrosis: An old term in search for a new meaning within the evolving concept of acute kidney injury

    New Horizons in Translational Medicine, Vol. 2, Núm. 4-5, pp. 110-117

  2. Plasma cardiotrophin-1 as a marker of hypertension and diabetes-induced target organ damage and cardiovascular risk

    Medicine (United States), Vol. 94, Núm. 30

  3. TGF-β/BMP proteins as therapeutic targets in renal fibrosis. Where have we arrived after 25 years of trials and tribulations?

    Pharmacology and Therapeutics, Vol. 156, pp. 44-58

2014

  1. ALK1 heterozygosity increases extracellular matrix protein expression, proliferation and migration in fibroblasts

    Biochimica et Biophysica Acta - Molecular Cell Research, Vol. 1843, Núm. 6, pp. 1111-1122

  2. Heterozygous disruption of activin receptor-like kinase 1 is associated with increased renal fibrosis in a mouse model of obstructive nephropathy

    Kidney International, Vol. 85, Núm. 2, pp. 319-332

  3. L-endoglin overexpression increases renal fibrosis after unilateral ureteral obstruction

    PLoS ONE, Vol. 9, Núm. 10

2012

  1. Functional specific roles of H-ras and N-ras. A proteomic approach using knockout cell lines

    Electrophoresis, Vol. 33, Núm. 9-10, pp. 1385-1396

2011

  1. net Etiopathology of chronic tubular, glomerular and renovascular nephropathies: Clinical implications

    Journal of Translational Medicine, Vol. 9

2010

  1. Analysis of K-Ras nuclear expression in fibroblasts and mesangial cells

    PLoS ONE, Vol. 5, Núm. 1

  2. Common pathophysiological mechanisms of chronic kidney disease: Therapeutic perspectives

    Pharmacology and Therapeutics, Vol. 128, Núm. 1, pp. 61-81

  3. Deletion of H-Ras decreases renal fibrosis and myofibroblast activation following ureteral obstruction in mice

    Kidney International, Vol. 77, Núm. 6, pp. 509-518

  4. Increased plasma soluble endoglin levels as an indicator of cardiovascular alterations in hypertensive and diabetic patients

    BMC Medicine, Vol. 8