The biochemical response of the heart to hypertension and exercise.
Trends Biochem Sci
; 29(11): 609-17, 2004 Nov.
Article
em En
| MEDLINE
| ID: mdl-15501680
ABSTRACT
Mechanical stress on the heart can lead to crucially different outcomes. Exercise is beneficial because it causes heart muscle cells to enlarge (hypertrophy). Chronic hypertension also causes hypertrophy, but in addition it causes an excessive increase in fibroblasts and extracellular matrix (fibrosis), death of cardiomyocytes and ultimately heart failure. Recent research shows that stimulation of physiological (beneficial) hypertrophy involves several signaling pathways, including those mediated by protein kinase B (also known as Akt) and the extracellular-signal-regulated kinases 1 and 2 (ERK1/2). Hypertension, beta-adrenergic stimulation and agonists such as angiotensin II (Ang II) activate not only ERK1/2 but also p38 and the Jun N-terminal kinase (JNK), leading to pathological heart remodeling. Despite this progress, the mechanisms that activate fibroblasts to cause fibrosis and those that differentiate between exercise and hypertension to produce physiological and pathological responses, respectively, remain to be established.
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Base de dados:
MEDLINE
Assunto principal:
Condicionamento Físico Animal
/
Exercício Físico
/
Hipertensão
/
Miocárdio
Tipo de estudo:
Etiology_studies
Limite:
Animals
/
Humans
Idioma:
En
Revista:
Trends Biochem Sci
Ano de publicação:
2004
Tipo de documento:
Article
País de afiliação:
Estados Unidos