Author: Ferreira, Anderson J.; Murça, Tatiane M.; Fraga-Silva, Rodrigo A.; Castro, Carlos Henrique; Raizada, Mohan K.; Santos, Robson A. S.
Title: New Cardiovascular and Pulmonary Therapeutic Strategies Based on the Angiotensin-Converting Enzyme 2/Angiotensin-(1–7)/Mas Receptor Axis Document date: 2012_1_26
ID: 0qkzd2w4_11
Snippet: Also, Ang-(1-7) inhibits serum-stimulated mitogen-activated protein kinase (MAPK) activation in cardiac myocytes [78] and prevents the Ang-II-mediated phosphorylation of ERK1/2 and Rho kinase in hearts in a dosedependent manner [79] . In line with these data, activation of endogenous ACE2 significantly reduced the phosphorylation of ERK1/2 in hearts of hypertensive rats (SHRs) [48] . However, Mercure et al. [19] reported that overexpression of An.....
Document: Also, Ang-(1-7) inhibits serum-stimulated mitogen-activated protein kinase (MAPK) activation in cardiac myocytes [78] and prevents the Ang-II-mediated phosphorylation of ERK1/2 and Rho kinase in hearts in a dosedependent manner [79] . In line with these data, activation of endogenous ACE2 significantly reduced the phosphorylation of ERK1/2 in hearts of hypertensive rats (SHRs) [48] . However, Mercure et al. [19] reported that overexpression of Ang-(1-7) in hearts of rats decreases the Ang-II-induced phosphorylation of c-Src and p38 kinase, whereas the increase in ERK1/2 phosphorylation was unaffected by the expression of the transgene, thereby suggesting a selective effect of Ang-(1-7) on intracellular signaling pathways related to cardiac remodeling.
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