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

Mitral Stenosis I: Introduction01:22

Mitral Stenosis I: Introduction

Mitral Valve Stenosis (MVS) is a heart condition where the mitral valve narrows, impeding blood circulation from the left atrium to the left ventricle. The etiology and pathophysiology of this condition are multifaceted, leading to a cascade of cardiovascular complications.Causes of Mitral Valve StenosisRheumatic Heart Disease: It is the main cause of mitral valve stenosis, particularly in developing nations. This condition arises from rheumatic fever, an inflammatory illness resulting from...

You might also read

Related Articles

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

Sort by
Same author

Echocardiographic assessment in arterial hypertension: a contemporary narrative review.

Echo research and practice·2026
Same author

<i>Kbtbd13</i> knockdown restores muscle function in a clinically relevant mouse model of nemaline myopathy type 6.

Science translational medicine·2026
Same author

RBM20 isoform regulation by independent transcription start sites adapts alternative splicing in development and disease.

Nature communications·2026
Same author

Titin's P-zone domains A164-167 are essential for thick filament structural arrangement.

The Journal of general physiology·2026
Same author

Rbm20 antisense oligonucleotides alleviate diastolic dysfunction in a mouse model of cardiometabolic heart failure (HFpEF).

Cardiovascular research·2025
Same author

Understanding Primary Care Dietitians' Experiences and Perspectives on Weight Management Practice Using the COM-B Model.

Journal of human nutrition and dietetics : the official journal of the British Dietetic Association·2025
Same journal

Edaravone Dexborneol regulates the endothelial PPARγ-PON1 axis to inhibit high-cholesterol-induced atherosclerosis.

Clinical science (London, England : 1979)·2026
Same journal

HDAC9 promotes atherosclerosis by suppressing CYP7A1 and impairing hepatic cholesterol excretion.

Clinical science (London, England : 1979)·2026
Same journal

Clusterin ameliorates LPS-induced ARDS by inhibiting the Wnt/β-catenin pathway.

Clinical science (London, England : 1979)·2026
Same journal

Human cytomegalovirus at the maternal-fetal interface: an overview of pathogenesis, defence, and interventions.

Clinical science (London, England : 1979)·2026
Same journal

Cardiometabolic regulation by adipocyte-derived leptin and the brain melanocortin system.

Clinical science (London, England : 1979)·2026
Same journal

Impact of impaired branched-chain amino acid metabolism on kidney disease.

Clinical science (London, England : 1979)·2026
See all related articles

Related Experiment Video

Updated: Jun 26, 2026

A Minimally Invasive Model of Aortic Stenosis in Swine
06:51

A Minimally Invasive Model of Aortic Stenosis in Swine

Published on: October 20, 2023

Titin isoform expression in aortic stenosis.

Lynne Williams1, Neil Howell, Domenico Pagano

  • 1Department of Cardiovascular Medicine, University of Birmingham, Birmingham, U.K. L.K.Williams@bham.ac.uk

Clinical Science (London, England : 1979)
|January 22, 2009
PubMed
Summary
This summary is machine-generated.

Patients with aortic stenosis show increased expression of the short N2B titin isoform, contributing to higher passive myocardial stiffness and potentially affecting cardiac performance during left ventricular pressure overload.

More Related Videos

Technique of Minimally Invasive Transverse Aortic Constriction in Mice for Induction of Left Ventricular Hypertrophy
08:34

Technique of Minimally Invasive Transverse Aortic Constriction in Mice for Induction of Left Ventricular Hypertrophy

Published on: September 25, 2017

Assessment of Cardiac Morphological and Functional Changes in Mouse Model of Transverse Aortic Constriction by Echocardiographic Imaging
09:05

Assessment of Cardiac Morphological and Functional Changes in Mouse Model of Transverse Aortic Constriction by Echocardiographic Imaging

Published on: June 21, 2016

Related Experiment Videos

Last Updated: Jun 26, 2026

A Minimally Invasive Model of Aortic Stenosis in Swine
06:51

A Minimally Invasive Model of Aortic Stenosis in Swine

Published on: October 20, 2023

Technique of Minimally Invasive Transverse Aortic Constriction in Mice for Induction of Left Ventricular Hypertrophy
08:34

Technique of Minimally Invasive Transverse Aortic Constriction in Mice for Induction of Left Ventricular Hypertrophy

Published on: September 25, 2017

Assessment of Cardiac Morphological and Functional Changes in Mouse Model of Transverse Aortic Constriction by Echocardiographic Imaging
09:05

Assessment of Cardiac Morphological and Functional Changes in Mouse Model of Transverse Aortic Constriction by Echocardiographic Imaging

Published on: June 21, 2016

Area of Science:

  • Cardiovascular Biology
  • Molecular Cardiology
  • Cardiac Mechanics

Background:

  • Titin is a crucial sarcomeric protein influencing myocardial stiffness.
  • The N2B titin isoform is associated with increased passive myocardial stiffness compared to the N2BA isoform.

Purpose of the Study:

  • To investigate the hypothesis that N2B titin isoform expression increases in aortic stenosis patients due to pressure overload.
  • To understand the role of titin isoforms in the hypertrophic response of the left ventricle.

Main Methods:

  • Myocardial biopsies from the left ventricle of 19 aortic stenosis patients and 13 donor hearts.
  • SDS-agarose gel electrophoresis to analyze cardiac titin isoforms (N2B and N2BA).

Main Results:

  • A significantly decreased N2BA/N2B titin isoform ratio was observed in aortic stenosis patients (0.48) compared to controls (0.66).
  • Total titin expression remained unchanged between the groups.
  • Increased N2B and decreased N2BA titin expression suggests a shift towards higher passive myocardial stiffness.

Conclusions:

  • Altered titin isoform expression (more N2B, less N2BA) in response to pressure overload may increase passive tension.
  • This alteration in titin isoforms could impact overall cardiac performance in aortic stenosis.