Related Experiment Video
Updated: Mar 9, 2026
12:42
Isolation of Retinal Arterioles for Ex Vivo Cell Physiology Studies
Published on: July 14, 2018
11.1K
Transient receptor potential vanilloid 2 function regulates cardiac hypertrophy via stretch-induced activation
Sheryl E Koch1, Adrien Mann, Shannon Jones
1aDepartment of Internal Medicine, Division of Cardiovascular Health and Disease bDepartment of Molecular and Cellular Physiology, University of Cincinnati, Cincinnati, Ohio, USA.
Journal of Hypertension
|December 24, 2016
Summary
Transient receptor potential vanilloid 2 subtype (TRPV2) channels regulate cardiomyocyte hypertrophy. Blocking TRPV2 function reduces left ventricular hypertrophy from increased afterload without impairing cardiac function.
Area of Science:
- Cardiovascular Physiology
- Molecular Biology
- Ion Channel Function
Background:
- Hypertension-induced afterload causes cardiomyocyte hypertrophy, leading to left ventricular hypertrophy and heart failure with preserved ejection fraction.
- The role of specific ion channels in mediating this hypertrophic response remains incompletely understood.
Purpose of the Study:
- To investigate the hypothesis that transient receptor potential vanilloid 2 subtype (TRPV2) function regulates cardiomyocyte hypertrophy under increased afterload conditions.
- To determine if TRPV2 plays a role in pressure overload-induced cardiac remodeling.
Main Methods:
- Utilized functional TRPV2 knockout mice and wild-type controls.
- Induced increased afterload via transverse aortic constriction (TAC).
- Assessed cardiac size, function (echocardiography, catheterization), and molecular markers of hypertrophy.
Main Results:
- TRPV2 expression was upregulated in wild-type hearts after TAC, localizing to the sarcolemmal membrane.
- TRPV2 knockout mice exhibited significantly reduced left ventricular hypertrophy following TAC.
- This reduction in hypertrophy was not observed with beta-adrenergic or angiotensin stimulation and did not compromise cardiac function.
Conclusions:
- TRPV2 functions as a stretch-activated channel that plays a critical role in regulating cardiomyocyte hypertrophy in response to increased afterload.
- Targeting TRPV2 may offer a therapeutic strategy for preventing or mitigating cardiac hypertrophy in hypertension.
Related Concept Videos
01:27Transducer Mechanism: Enzyme-Linked Receptors
4.6K
Enzyme-linked receptors are cell-surface receptors acting as an enzyme or associating with an enzyme intracellularly. They make excellent drug targets. Drugs can bind to the extracellular ligand-binding domain or directly affect their enzymatic domain and alter their activity.
Major types that are helpful drug targets include:
Major types that are helpful drug targets include:
4.6K
01:29Heart Failure II: Pathophysiology
1.2K
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...
1.2K
01:21G-Protein Gated Ion Channels
6.5K
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...
Sensory...
6.5K
01:12Mechanically-gated Ion Channels
8.0K
Mechanically-gated ion channels are proteins found in eukaryotic and prokaryotic cell membranes that open in response to mechanical stress. Tension, compression, swelling, and shear stress can alter the conformation of the protein, opening a transmembrane channel that allows the passage of ions for signal transmission. In eukaryotes, mechanically-gated channels are distributed in several regions like the neurons, lungs, skin, bladder, and heart, where they play critical roles in numerous...
8.0K
01:26Tension Response at Adherens Junctions
3.9K
The adherens junctions that anchor cells together are multi-protein complexes that dynamically adapt to mechanical stimuli such as tensile forces and shear stress. Mechanosensory proteins in these junctions can sense such mechanical stimuli and undergo a shift in their conformation, resulting in an altered function — a process called mechanotransduction.
α-Catenin as a Mechanosensory Protein
The α-catenin of adherens junctions is an allosteric protein with three VH (vinculin...
α-Catenin as a Mechanosensory Protein
The α-catenin of adherens junctions is an allosteric protein with three VH (vinculin...
3.9K
01:25Smooth Muscle Contraction
8.8K
Smooth muscle contraction is a complex process vital for various bodily functions, from maintaining blood vessel tension to facilitating the movement of food through the digestive tract. Unlike striated muscles, smooth muscle contraction begins more slowly and lasts longer.
The onset of contraction is triggered by an increase in calcium ions within the sarcoplasm, similar to the process in striated muscle. However, smooth muscles have a relatively smaller reservoir of the sarcoplasmic...
The onset of contraction is triggered by an increase in calcium ions within the sarcoplasm, similar to the process in striated muscle. However, smooth muscles have a relatively smaller reservoir of the sarcoplasmic...
8.8K