Zobrazeno 1 - 10
of 35
pro vyhledávání: '"Claudia I. Caldiz"'
Autor:
María S. Brea, Romina G. Díaz, Daiana S. Escudero, Claudia I. Caldiz, Enrique L. Portiansky, Patricio E. Morgan, Néstor G. Pérez
Publikováno v:
Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease, Vol 5, Iss 10 (2016)
BackgroundMyocardial stretch increases force biphasically: the Frank‐Starling mechanism followed by the slow force response (SFR). Based on pharmacological strategies, we proposed that epidermal growth factor (EGF) receptor (EGFR or ErbB1) activati
Externí odkaz:
https://doaj.org/article/6b9aa375073f461d9f2d732464ea3288
Autor:
Joshua Godoy Coto, Erica Pereyra, Fiorella Cavalli, Claudia I. Caldiz, Alejandra M. Yeves, Irene L. Ennis
Publikováno v:
Journal of Molecular and Cellular Cardiology. 173:4
Autor:
Alejandra M. Yeves, Joshua Godoy Coto, Fiorella Cavalli, Erica Pereyra, Claudia I. Caldiz, Irene L. Ennis
Publikováno v:
Journal of Molecular and Cellular Cardiology. 173:131
Autor:
Fiorella Cavalli, Claudia I. Caldiz, Alejandra M. Yeves, Irene L. Ennis, Joshua Godoy Coto, Erica Pereyra
Publikováno v:
The FASEB Journal. 35
Autor:
Enrique Leo Portiansky, María E. Amarillo, Néstor G. Pérez, María Soledad Brea, Claudia I. Caldiz, Daiana S. Escudero, Jorge Oswaldo Aranda, Romina Gisel Díaz
Publikováno v:
European journal of pharmacology. 891
Previously, we have shown that an increased cGMP-activated protein Kinase (PKG) activity after phosphodiesterase 5 (PDE5) inhibition by Sildenafil (SIL), leads to myocardial Na+/H+ exchanger (NHE1) inhibition preserving its basal homeostatic function
Autor:
María S, Brea, Romina G, Díaz, Daiana S, Escudero, Maite R, Zavala, Enrique L, Portiansky, María C, Villa-Abrille, Claudia I, Caldiz, Néstor G, Pérez, Patricio E, Morgan
Publikováno v:
Biochemical pharmacology. 170
Pathological cardiac hypertrophy (PCH) can be triggered by epidermal growth factor receptor (EGFR) transactivation. Progression of PCH can be prevented by inhibition of hyperactive Na
Autor:
Oscar Andres Pinilla, Claudia I. Caldiz, Irene L. Ennis, Andrés J. Medina, Enrique Leo Portiansky
Publikováno v:
CONICET Digital (CONICET)
Consejo Nacional de Investigaciones Científicas y Técnicas
instacron:CONICET
Consejo Nacional de Investigaciones Científicas y Técnicas
instacron:CONICET
Chronic activation of the renin angiotensin system (RAS) favors several cardiac diseases, among which myocardial hypertrophy occupies an outstanding place. In this context, the hyperactivity of the cardiac Na+/H+ (NHE-1) exchanger plays a key role. T
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::6dd626f1444ccb343fa1060163eb9bad
https://www.sciencedirect.com/science/article/abs/pii/S0014480018303691
https://www.sciencedirect.com/science/article/abs/pii/S0014480018303691
Autor:
Susana M. Mosca, Juliana Catalina Fantinelli, José Luis Ríos, Luisa Fernanda González Arbeláez, Claudia I. Caldiz, Alejandro Ciocci Pardo, Guillermo Raúl Schinella
Publikováno v:
CONICET Digital (CONICET)
Consejo Nacional de Investigaciones Científicas y Técnicas
instacron:CONICET
Consejo Nacional de Investigaciones Científicas y Técnicas
instacron:CONICET
Our objective was to determine the effects of a polyphenol-enriched cocoa extract (PCE) on myocardial postischemic alterations in normotensive (Wistar rats, W) and spontaneously hypertensive rats (SHR). Isolated hearts were submitted to 110 min of pe
Autor:
Daiana S. Escudero, María Soledad Brea, Romina Gisel Díaz, María C. Villa-Abrille, Patricio E. Morgan, Maite Zavala, Enrique Leo Portiansky, Néstor G. Pérez, Claudia I. Caldiz
Publikováno v:
Biochemical Pharmacology. 170:113667
Pathological cardiac hypertrophy (PCH) can be triggered by epidermal growth factor receptor (EGFR) transactivation. Progression of PCH can be prevented by inhibition of hyperactive Na+/H+ exchanger isoform 1 (NHE1). We first aimed, to limit PCH of sp
Publikováno v:
Experimental and molecular pathology. 107
Chronic activation of the renin angiotensin system (RAS) favors several cardiac diseases, among which myocardial hypertrophy occupies an outstanding place. In this context, the hyperactivity of the cardiac Na