| dc.creator | Cingolani, Horacio Eugenio | |
| dc.creator | Camilión de Hurtado, María Cristina | |
| dc.date | 2002 | |
| dc.date | 2019-11-05T16:39:16Z | |
| dc.identifier | http://sedici.unlp.edu.ar/handle/10915/84978 | |
| dc.identifier | issn:0009-7330 | |
| dc.description | Cardiac 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.description | Facultad de Ciencias Médicas | |
| dc.description | Centro de Investigaciones Cardiovasculares | |
| dc.format | application/pdf | |
| dc.format | 751-753 | |
| dc.language | en | |
| dc.rights | http://creativecommons.org/licenses/by-nc-sa/4.0/ | |
| dc.rights | Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0) | |
| dc.subject | Ciencias Médicas | |
| dc.subject | Cardiac hypertrophy | |
| dc.subject | Na+-H+ exchanger | |
| dc.subject | NHE1 inhibitors | |
| dc.title | Na+-H+ exchanger inhibition : A new antihypertrophic tool | |
| dc.type | Articulo | |
| dc.type | Articulo | |
