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January 1, 1994Journal of Biological ChemistryOpen Access

Endothelin-1 and fibroblast growth factors stimulate the mitogen-activated protein kinase signaling cascade in cardiac myocytes. The potential role of the cascade in the integration of two signaling pathways leading to myocyte hypertrophy.

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Population

Cultured myocytes from neonatal rat heart ventricles

Comparison

Endothelin-1, acidic FGF, or… vs Control (unstimulated cells)

Design

Preclinical

Follow-up

Up to 24 hours

Authors

MBMarie A. BogoyevitchPGPeter E. GlennonMAMonica Andersson

Discussion

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Overview

MAPK convergence by ET-1/aFGF may contribute to myocyte hypertrophy; leaves open causal role in vivo and clinical relevance.

Structured PICO

P
Population
Cultured myocytes from neonatal rat heart ventricles
I
Intervention
Endothelin-1 (ET-1), acidic FGF (aFGF), or 12-O-tetradecanoylphorbol-13-acetate (TPA)
C
Comparator
Control (unstimulated cells)
O
Outcome
Activation of mitogen-activated protein kinase (MAPK) and MAPK kinase (MAPKK)surrogate

Dissimilar signaling pathways activated by ET-1 and aFGF converge at the MAPKK/MAPK cascade, which may play a role in cardiac myocyte hypertrophy.

Cite This Study

Bogoyevitch et al. (1994) studied this question.

synapsesocial.com/papers/69d570ee75589c71d767e03ahttps://doi.org/10.1016/s0021-9258(17)42228-9
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