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G protein-coupled receptor signalling in in vivo cardiac overload
A Rapacciuolo1, G Esposito, S V Prasad
1Department of Medicine, Duke University Medical Center, Durham, NC 27710, USA.
Insights
Cardiac cells enlarge due to stress, a process linked to heart problems. This review explores G protein-coupled receptors and signaling pathways involved in cardiac hypertrophy and failure.
Area of Science:
- Cardiology
- Cellular Biology
- Molecular Biology
Background:
- Cardiac myocytes undergo hypertrophy in response to biomechanical stress.
- Cardiac hypertrophy is linked to increased catecholamines, morbidity, and mortality.
- Understanding hypertrophy's initiation is crucial for preventing heart failure.
Purpose of the Study:
- To review the role of G protein-coupled receptors in cardiac hypertrophy.
- To explore signaling pathways activated by these receptors in the heart.
Main Methods:
- Literature review focusing on G protein-coupled receptors.
- Analysis of signaling pathways including MAPK and PI3K.
Main Results:
- G protein-coupled receptors are key initiators of cardiac hypertrophy.
- Activation of MAPK and PI3K pathways by GPCRs contributes to hypertrophic response.
Conclusions:
- GPCRs play a significant role in the cellular signaling of cardiac hypertrophy.
- Targeting GPCRs and associated pathways may offer therapeutic strategies for heart failure.
Abstract:
Cardiac myocytes respond to biomechanical stress by initiating cellular processes that lead to hypertrophy. Although cardiac hypertrophy is a response to increased stress on the heart, it is associated with elevated plasma catecholamine levels and an increase in cardiac morbidity and mortality. Understanding the cellular signals that initiate the hypertrophic response will be of critical importance to identify pathways that mediate the maladaptive deterioration of the hypertrophic heart to one of cardiac failure. This review will focus on the role of G protein-coupled receptors in the activation of signalling pathways in the heart, such as the mitogen activated protein kinase and phosphoinositide-3 kinase pathways.