Carlos Zaragoza Sánchez-rekin lankidetzan egindako argitalpenak (52)

2024

  1. Indoxyl Sulfate-Induced Valve Endothelial Cell Endothelial-to-Mesenchymal Transition and Calcification in an Integrin-Linked Kinase-Dependent Manner

    Cells, Vol. 13, Núm. 6

  2. NOS3 prevents MMP-9, and MMP-13 induced extracellular matrix proteolytic degradation through specific microRNA-targeted expression of extracellular matrix metalloproteinase inducer in hypertension-related atherosclerosis

    Journal of Hypertension, Vol. 42, Núm. 4, pp. 685-693

  3. Novel cutting edge nano-strategies to address old long-standing complications in cardiovascular diseases. A comprehensive review

    European Journal of Clinical Investigation, Vol. 54, Núm. 7

  4. Replicative Endothelial Cell Senescence May Lead to Endothelial Dysfunction by Increasing the BH2/BH4 Ratio Induced by Oxidative Stress, Reducing BH4 Availability, and Decreasing the Expression of eNOS

    International Journal of Molecular Sciences, Vol. 25, Núm. 18

2023

  1. Endothelial ILK induces cardioprotection by preventing coronary microvascular dysfunction and endothelial-to-mesenchymal transition

    Basic research in cardiology, Vol. 118, Núm. 1, pp. 28

  2. Endothelial integrine-linked kinase and valvular calcification: Molecular study of calcification in aortic valve

    Cirugia Cardiovascular, Vol. 30, Núm. 1, pp. 11-16

2022

  1. Aging-related ILK levels are associated with calcified aortic valve and circulating miR 199-3p levels

    Revista Espanola de Cardiologia, Vol. 75, Núm. 1, pp. 88-91

  2. Comparison of the renal effects of bisphenol A in mice with and without experimental diabetes. Role of sexual dimorphism

    Biochimica et Biophysica Acta - Molecular Basis of Disease, Vol. 1868, Núm. 1

  3. Corrigendum: Preclinical models of congestive heart failure, advantages and limitations for application in clinical practice (Front. Physiol., (2022), 13, 850301, 10.3389/fphys.2022.850301)

    Frontiers in Physiology

  4. Integrin-Linked Kinase Expression in Human Valve Endothelial Cells Plays a Protective Role in Calcific Aortic Valve Disease

    Antioxidants, Vol. 11, Núm. 9

  5. NIL10: A New IL10-Receptor Binding Nanoparticle That Induces Cardiac Protection in Mice and Pigs Subjected to Acute Myocardial Infarction through STAT3/NF-κB Activation

    Pharmaceutics, Vol. 14, Núm. 10

  6. Preclinical models of congestive heart failure, advantages, and limitations for application in clinical practice

    Frontiers in Physiology, Vol. 13

  7. Theranostic Contribution of Extracellular Matrix Metalloprotease Inducer-Paramagnetic Nanoparticles Against Acute Myocardial Infarction in a Pig Model of Coronary Ischemia-Reperfusion

    Circulation. Cardiovascular imaging, Vol. 15, Núm. 6, pp. e013379

2021

  1. Cardiac microvasculature and adverse remodeling after acute myocardial infarction. New evidence on the use of VEGF as a therapeutic target

    Revista Espanola de Cardiologia, Vol. 74, Núm. 2, pp. 124-125

  2. Ivabradine induces cardiac protection against myocardial infarction by preventing cyclophilin‐a secretion in pigs under coronary ischemia/reperfusion

    International Journal of Molecular Sciences, Vol. 22, Núm. 6, pp. 1-13

  3. Ivabradine induces cardiac protection by preventing cardiogenic shock-induced extracellular matrix degradation

    Revista Espanola de Cardiologia, Vol. 74, Núm. 12, pp. 1063-1072

  4. miR-16 induces endoplasmic reticulum stress in ischemic dilated cardiomyopathy

    Revista Espanola de Cardiologia, Vol. 74, Núm. 9, pp. 732-733

2020

  1. Bisphenol A induces coronary endothelial cell necroptosis by activating RIP3/CamKII dependent pathway

    Scientific Reports, Vol. 10, Núm. 1

  2. Ivabradine in acute heart failure: Effects on heart rate and hemodynamic parameters in a randomized and controlled swine trial

    Cardiology Journal, Vol. 27, Núm. 1, pp. 62-71

  3. Ivabradine-stimulated microvesicle release induces cardiac protection against acute myocardial infarction

    International Journal of Molecular Sciences, Vol. 21, Núm. 18, pp. 1-12