Nestor G Perez
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Explore the profile of Nestor G Perez including associated specialties, affiliations and a list of published articles.
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Recent Articles
11.
Sepulveda D, Cabeza Meckert P, Locatelli P, Olea F, Perez N, Pinilla O, et al.
Cytotechnology
. 2014 Nov;
68(4):665-74.
PMID: 25432330
The adult heart contains a population of cardiac progenitor cells (CPCs). Growing and collecting an adequate number of CPCs demands complex culture media containing growth factors. Since activated macrophages secrete...
12.
Yeves A, Villa-Abrille M, Perez N, Medina A, Escudero E, Ennis I
J Mol Cell Cardiol
. 2014 Sep;
76:186-95.
PMID: 25240639
Background: The involvement of NHE-1 hyperactivity, critical for pathological cardiac hypertrophy (CH), in physiological CH has not been elucidated yet. Stimulation of NHE-1 increases intracellular Na(+) and Ca(2+) favouring calcineurin...
13.
Diaz R, Perez N, Morgan P, Villa-Abrille M, Caldiz C, Nolly M, et al.
Hypertension
. 2013 Oct;
63(1):112-8.
PMID: 24126173
Myocardial stretch triggers an angiotensin II-dependent autocrine/paracrine loop of intracellular signals, leading to reactive oxygen species-mediated activation of redox-sensitive kinases. Based on pharmacological strategies, we previously proposed that mineralocorticoid receptor...
14.
Ennis I, Aiello E, Cingolani H, Perez N
Curr Cardiol Rev
. 2013 Aug;
9(3):230-40.
PMID: 23909633
The stretch of cardiac muscle increases developed force in two phases. The first phase, which occurs rapidly, constitutes the well-known Frank-Starling mechanism and it is generally attributed to enhanced myofilament...
15.
Vargas L, Diaz R, Swenson E, Perez N, Alvarez B
Am J Physiol Heart Circ Physiol
. 2013 May;
305(2):H228-37.
PMID: 23709596
Myocardial stretch is an established signal that leads to hypertrophy. Myocardial stretch induces a first immediate force increase followed by a slow force response (SFR), which is a consequence of...
16.
Cingolani H, Perez N, Cingolani O, Ennis I
Am J Physiol Heart Circ Physiol
. 2012 Nov;
304(2):H175-82.
PMID: 23161880
Myocardial stretch elicits a rapid increase in developed force, which is mainly caused by an increase in myofilament calcium sensitivity (Frank-Starling mechanism). Over the ensuing 10-15 min, a second gradual...
17.
Caldiz C, Diaz R, Nolly M, de Cingolani G, Ennis I, Cingolani H, et al.
J Physiol
. 2011 Dec;
589(Pt 24):6051-61.
PMID: 22174146
The increase in myocardial reactive oxygen species after epidermal growth factor receptor transactivation is a crucial step in the autocrine/paracrine angiotensin II/endothelin receptor activation leading to the slow force response...
18.
Cingolani O, Perez N, Ennis I, Alvarez M, Mosca S, Schinella G, et al.
Pflugers Arch
. 2011 Aug;
462(5):733-43.
PMID: 21870055
Growing in vitro evidence suggests NHE-1, a known target for reactive oxygen species (ROS), as a key mediator in cardiac hypertrophy (CH). Moreover, NHE-1 inhibition was shown effective in preventing...
19.
Perez N, Nolly M, Roldan M, Villa-Abrille M, Cingolani E, Portiansky E, et al.
J Appl Physiol (1985)
. 2011 Jun;
111(3):874-80.
PMID: 21659487
Myocardial stretch induces a biphasic force response: a first abrupt increase followed by a slow force response (SFR), believed to be the in vitro manifestation of the Anrep effect. The...
20.
Morgan P, Correa M, Ennis I, Ennis I, Diez A, Perez N, et al.
J Appl Physiol (1985)
. 2011 May;
111(2):566-72.
PMID: 21596922
Cardiac Na(+)/H(+) exchanger (NHE1) hyperactivity is a central factor in cardiac remodeling following hypertension, myocardial infarction, ischemia-reperfusion injury, and heart failure. Treatment of these pathologies by inhibiting NHE1 is challenging...