Related Experiment Video

Updated: Sep 21, 2026

A Kinetic Fluorescence-based Ca2+ Mobilization Assay to Identify G Protein-coupled Receptor Agonists, Antagonists, and Allosteric Modulators
07:41

A Kinetic Fluorescence-based Ca2+ Mobilization Assay to Identify G Protein-coupled Receptor Agonists, Antagonists, and Allosteric Modulators

Published on: February 20, 2018

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.

Acta Physiologica Scandinavica
|October 27, 2001
PubMed

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.

More Related Videos

Magnetic Adjustment of Afterload in Engineered Heart Tissues09:40

Magnetic Adjustment of Afterload in Engineered Heart Tissues

Published on: May 5, 2020

Surgically Induced Cardiac Volume Overload by Aortic Regurgitation in Mouse08:12

Surgically Induced Cardiac Volume Overload by Aortic Regurgitation in Mouse

Published on: August 30, 2022

Related Concept Videos

G Protein-coupled Receptors01:27

G Protein-coupled Receptors

G-protein-coupled receptors are ligand-binding receptors that indirectly affect changes in the cell. The actual receptor is a single polypeptide that traverses the cell membrane seven times, creating intracellular and extracellular loops. The extracellular loops create a ligand-specific pocket which binds to neurotransmitters or hormones. The intracellular loops hold onto the G-protein.The G-protein, or guanine nucleotide-binding protein, is a large heterotrimeric complex. Its three subunits...
G Protein-coupled Receptors01:15

G Protein-coupled Receptors

G Protein-Coupled Receptors or GPCRs are membrane-bound receptors that transiently associate with heterotrimeric G proteins and induce an appropriate response to sensory stimuli such as light, odors, hormones, cytokines, or neurotransmitters.
GPCRs are also called heptahelical, 7TM, or serpentine receptors, and consist of seven (H1-H7) transmembrane alpha-helices that span the bilayer to form a cylindrical core. The transmembrane helices are connected by three extracellular loops and three...
GPCR Desensitization01:12

GPCR Desensitization

G protein-coupled receptor (GPCR) signaling plays a crucial role in cell functioning. GPCR desensitization is an equally essential process. It allows cells to respond to changing environments and regain sensitivity to new stimuli while preventing unnecessary stimulation when no longer needed. Prolonged exposure to stimuli leads to GPCR desensitization. It involves blocking the receptors from binding and activating additional G proteins. This inhibits activation of downstream effectors, thereby...
G-Protein Gated Ion Channels01:21

G-Protein Gated Ion Channels

GPCRs are primarily responsible for our sense of smell, taste, and vision.  The binding of a sensory stimulus activates GPCR to stimulate effector proteins, many of which are ion channels in the sensory organs. GPCRs modulate the opening and closing of the target ion channels either directly by binding them, or by releasing second messengers that activate these channels. As ions move across the membrane, the membrane potential is altered, which induces an appropriate response.
Sensory organs,...
GPCRs Regulate Adenylyl Cylase Activity01:09

GPCRs Regulate Adenylyl Cylase Activity

Some GPCRs transmit signals through adenylyl cyclase (AC), a transmembrane enzyme. AC helps synthesize second messenger cyclic adenosine monophosphate (cAMP). AC catalyzes cyclization reaction and converts ATP to cAMP by releasing a pyrophosphate. The pyrophosphate is further hydrolyzed to phosphate by the enzyme pyrophosphatase, which drives cAMP synthesis to completion. However, cAMP is rapidly degraded to 5′ AMP by the enzymes phosphodiesterase (PDE), preventing overstimulation of cells.
Two...
Heart Failure II: Pathophysiology01:29

Heart Failure II: Pathophysiology

Systolic Heart Failure and Compensatory MechanismsSystolic heart failure (also termed HFrEF, Heart Failure with Reduced Ejection Fraction) is the most prevalent type of heart filure. It results in a decreased volume of blood being pumped from the ventricle. The aortic arch and carotid sinuses have baroreceptors that detect reduced blood pressure, triggering the sympathetic nervous system (SNS) to release epinephrine and norepinephrine. Initially, this response aims to boost heart rate and...