Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Cardiomyopathy II: Dilated Cardiomyopathy01:30

Cardiomyopathy II: Dilated Cardiomyopathy

549
Dilated cardiomyopathy, or DCM, is a progressive myocardial disorder characterized by ventricular chamber dilation and contractile dysfunction.EtiologyVarious factors can cause DCM, including hypertension and heavy alcohol intake, which contribute to the weakening and enlargement of the heart muscle. Viral infections, such as Coxsackievirus B, adenoviruses, and influenza, can lead to DCM by causing inflammation and damage to heart tissue. Certain chemotherapeutic agents, including daunorubicin,...
549
Cardiomyopathy III: Hypertrophic Cardiomyopathy01:29

Cardiomyopathy III: Hypertrophic Cardiomyopathy

467
Hypertrophic cardiomyopathy, or HCM, is an autosomal dominant genetic disorder characterized by asymmetric left ventricular hypertrophy without ventricular dilation. It is more common in men and is typically diagnosed in young, athletic adults.EtiologyHCM is primarily genetic and is caused by mutations in genes encoding sarcomeric proteins. Researchers have identified over 1400 mutations across at least 11 different genes. Among these, the most frequently occurring mutations are found in the...
467
Cardiomyopathy IV: Restrictive Cardiomyopathy01:29

Cardiomyopathy IV: Restrictive Cardiomyopathy

519
Restrictive cardiomyopathy (RCM) is a rare heart muscle disease characterized by impaired ventricular filling due to stiffened ventricular walls, leading to significant diastolic dysfunction.EtiologyRestrictive cardiomyopathy can arise from both inherited and acquired diseases, many of which are systemic. It is categorized into four main types: infiltrative, storage, non-infiltrative, and endomyocardial diseases.Infiltrative diseases, such as amyloidosis, lead to RCM by depositing amyloid...
519
Gain01:15

Gain

407
Gain and phase shift are properties of linear circuits that describe the effect a circuit has on a sinusoidal input voltage or current. The circuit's behavior that contains reactive elements will depend on the frequency of the input sinusoid. As a result, it is observed that the gain and phase shift will all be frequency functions.
Gain:
Suppose Vin is the input and Vout is the output signal to a circuit.
407
Histone Variants at the Centromere02:30

Histone Variants at the Centromere

5.0K
Histone variants are the histone proteins with structural and sequence variations. These variants may be regarded as “mutant” forms that replace their canonical histone counterparts in the nucleosomes. Specific post-translational modifications on the histone variants enable further chromatin complexity and regulate tissue-specific gene expression. The most common histone variants are from histone H2A, H2B, and linker histone H1 families. However, several variants of histone H3...
5.0K
Cardiomyopathy V: Interprofessional Care01:29

Cardiomyopathy V: Interprofessional Care

396
Managing cardiomyopathy involves addressing underlying or precipitating causes, treating heart failure with medications, and implementing dietary changes and a balanced exercise and rest regimen.Lifestyle ModificationsCardiomyopathy patients should adopt a low-sodium diet to reduce fluid retention and manage heart failure. A personalized exercise and rest plan helps maintain physical fitness without overstraining the heart. Avoiding alcohol and tobacco is essential to prevent further damage to...
396

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Spermidine ameliorates BK channel dysfunction in diabetic coronary smooth muscle cells via PKM2/STAT3/FBXO32 axis.

Vascular pharmacology·2026
Same author

Channel and Spatial Parallel Attention for ECG-Based Prediction of Concealed Accessory Pathways and Atrioventricular Nodal Reentry Tachycardia.

Journal of arrhythmia·2026
Same author

Clinical Risks and Underlying Mechanisms of Atrial Fibrillation after Myocardial Infarction.

Current cardiology reviews·2026
Same author

Correction: A comparable efficacy and safety between intracardiac echocardiography and transesophageal echocardiography for percutaneous left atrial appendage occlusion.

Frontiers in cardiovascular medicine·2026
Same author

Synergistic Enhancement of Diosgenin Dissolution and Bioavailability via Ternary Solid Dispersions and Self-Assembled Polymeric Micelles.

Drug design, development and therapy·2026
Same author

Functional evaluation of TRPC6 missense variants in cancer patients via molecular docking analysis compared with patch Clamp electrophysiology.

The Journal of biological chemistry·2026

Related Experiment Video

Updated: Jan 29, 2026

A Doxorubicin-Induced Murine Model of Dilated Cardiomyopathy In Vivo
05:14

A Doxorubicin-Induced Murine Model of Dilated Cardiomyopathy In Vivo

Published on: May 16, 2020

5.3K

Gain-of-Function Variant TRPC6 A404V Is Associated With Doxorubicin-Related Cardiomyopathy.

Ying Wu1,2, Xiaojing Sun1, Ru-Xing Wang2

  • 1Department of Cardiovascular Medicine, Mayo Clinic, Rochester, MN (Y.W., X.S., H.-C.L., T.L.).

Circulation. Genomic and Precision Medicine
|January 28, 2026
PubMed
Summary

The TRPC6 A404V variant increases risk for doxorubicin-induced cardiomyopathy by enhancing channel activity. This gain-of-function variant shows increased expression and response to doxorubicin, highlighting its role in cardiotoxicity.

Keywords:
anthracyclinecalcineurincardiotoxicityglycerolhomeostasis

More Related Videos

A Doxorubicin-induced Cardiomyopathy Model in Adult Zebrafish
08:09

A Doxorubicin-induced Cardiomyopathy Model in Adult Zebrafish

Published on: June 7, 2018

10.3K
A Scalable, Cell-Based Method for the Functional Assessment of Ube3a Variants
06:35

A Scalable, Cell-Based Method for the Functional Assessment of Ube3a Variants

Published on: October 10, 2022

2.4K

Related Experiment Videos

Last Updated: Jan 29, 2026

A Doxorubicin-Induced Murine Model of Dilated Cardiomyopathy In Vivo
05:14

A Doxorubicin-Induced Murine Model of Dilated Cardiomyopathy In Vivo

Published on: May 16, 2020

5.3K
A Doxorubicin-induced Cardiomyopathy Model in Adult Zebrafish
08:09

A Doxorubicin-induced Cardiomyopathy Model in Adult Zebrafish

Published on: June 7, 2018

10.3K
A Scalable, Cell-Based Method for the Functional Assessment of Ube3a Variants
06:35

A Scalable, Cell-Based Method for the Functional Assessment of Ube3a Variants

Published on: October 10, 2022

2.4K

Area of Science:

  • Cardiology
  • Genetics
  • Pharmacology

Background:

  • TRPC6 channels are crucial for cardiac calcium homeostasis.
  • TRPC6 variants are linked to chemotherapy-induced cardiomyopathy.
  • The TRPC6 A404V polymorphism is found in patients receiving anthracycline therapy.

Purpose of the Study:

  • To investigate the mechanisms by which the TRPC6 A404V variant contributes to doxorubicin-related cardiomyopathy.
  • To assess the effects of doxorubicin and doxorubicinol on TRPC6 A404V channel function and expression.

Main Methods:

  • Patch-clamp recordings and Ca2+ imaging were used to assess channel function.
  • Molecular biology techniques and computational analysis were employed.
  • Experiments were conducted in heterologous systems and native cardiac cells.

Main Results:

  • The TRPC6 A404V variant showed increased membrane expression and potentiated channel activity.
  • Doxorubicin enhanced TRPC6 mRNA expression and channel function, particularly in A404V variants.
  • Computational modeling indicated the A404V mutation alters OAG binding, enhancing channel activation.

Conclusions:

  • TRPC6 A404V is a gain-of-function variant with enhanced activity in the presence of doxorubicin.
  • The TRPC6 A404V variant is a risk factor for anthracycline-induced cardiotoxicity.
  • Understanding this mechanism may inform strategies to mitigate chemotherapy-related heart damage.