dc.creatorCingolani, Horacio Eugenio
dc.creatorCamilión de Hurtado, María Cristina
dc.date2002
dc.date2019-11-05T16:39:16Z
dc.identifierhttp://sedici.unlp.edu.ar/handle/10915/84978
dc.identifierissn:0009-7330
dc.descriptionCardiac hypertrophy (CH) is a major risk factor for cardiac death and commonly precedes the development of heart failure (HF). This is motivating the search for novel pharmacological strategies to prevent the development and/or regress CH. Although the signaling pathways leading to myocardial hypertrophy are complex, one important set of pathways involves the mitogen-activated protein kinases (MAPKs). MAPKs phosphorylate numerous substrates, including nuclear transcription factors that activate the expression of different genes. The Na<SUP>+</SUP>-H<SUP>+</SUP> exchanger (NHE) is a common downstream effector of this cascade and has been implicated in different models of hypertrophy, such as “hypertensive” myocardium, aortic constrictioninduced hypertrophy, and postinfarction myocardial hypertrophy. Interestingly, stretch-induced hypertrophy of cultured neonatal cardiomyocytes is also accompanied by an increase in MAPK activity and NHE activation. Furthermore, stretch-induced MAPK stimulation is partially prevented by inhibition of NHE activity.
dc.descriptionFacultad de Ciencias Médicas
dc.descriptionCentro de Investigaciones Cardiovasculares
dc.formatapplication/pdf
dc.format751-753
dc.languageen
dc.rightshttp://creativecommons.org/licenses/by-nc-sa/4.0/
dc.rightsCreative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0)
dc.subjectCiencias Médicas
dc.subjectCardiac hypertrophy
dc.subjectNa+-H+ exchanger
dc.subjectNHE1 inhibitors
dc.titleNa+-H+ exchanger inhibition : A new antihypertrophic tool
dc.typeArticulo
dc.typeArticulo


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