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

Aneurysm I: Introduction01:30

Aneurysm I: Introduction

40
An aortic aneurysm is a localized outpouching or dilation at a weak point in the artery wall. It may involve different parts of the aorta, such as the abdominal aorta, aortic arch, or thoracic aorta.Etiological factorsSeveral disorders are associated with aortic aneurysms.Congenital causes, such as primary connective tissue disorders like Marfan syndrome, impact the integrity and strength of connective tissues, notably affecting the aorta. Marfan syndrome is a genetic disorder that specifically...
40
Mitral Valve Prolapse I: Introduction01:27

Mitral Valve Prolapse I: Introduction

63
IntroductionThe mitral valve, one of the heart's four valves, regulates blood flow. These valves have flaps that open and close to direct blood properly through the heart and body. During each heartbeat, the flaps open for blood to pass through and seal shut to prevent backflow. Specifically, the mitral valve opens to allow blood flow from the heart's upper left chamber to the lower left chamber. It then closes securely as the lower left chamber contracts to pump blood to the body, preventing...
63
Aortic Regurgitation I: Introduction01:15

Aortic Regurgitation I: Introduction

67
IntroductionAortic regurgitation is characterized by the backward flow of blood from the aorta into the left ventricle during diastole and arises from the improper closure of the aortic valve. This condition results in left ventricular volume overload and can stem from both acute and chronic etiologies, each contributing uniquely to the disease's progression and symptomatology.Acute and Chronic CausesAcute aortic regurgitation often results from events that suddenly impair the integrity of the...
67
Mitral Stenosis I: Introduction01:22

Mitral Stenosis I: Introduction

80
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...
80
Atherosclerosis I: Introduction01:30

Atherosclerosis I: Introduction

157
Atherosclerosis is a progressive disorder characterized by the buildup of plaques on the arterial inner wall, causing them to narrow and harden over time. These plaques comprise lipids, calcium, blood components, carbohydrates, and fibrous tissue. The process primarily affects the intima of large and medium-sized arteries, reducing blood flow in any artery.Etiology and risk factorsThe cause of atherosclerosis is multifactorial, involving a complex interplay among endothelial injury, lipid...
157
Mitral Regurgitation I: Introduction01:20

Mitral Regurgitation I: Introduction

77
Mitral regurgitation is characterized by the backward circulation of blood from the left ventricle to the left atrium during systole, a phase of the cardiac cycle when the heart contracts and pumps blood out of the chambers. This abnormal flow occurs primarily due to the dysfunction of the mitral valve or its supporting structures, which include the mitral leaflets, chordae tendineae, annulus, and papillary muscles.Etiology and Mechanisms:Primary Mitral Regurgitation: This type arises from...
77

You might also read

Related Articles

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

Sort by
Same author

Fibronectin-induced overactivation of α<sub>V</sub>β<sub>3</sub>-PI3K-PIP3-PDK1-ILK signaling drives aortic disease in Marfan syndrome.

Nature communications·2026
Same author

Mechanics and mechanobiology of arterial development.

Biomechanics and modeling in mechanobiology·2026
Same author

Microstructural and Biomechanical Determinants of Biological Aging.

bioRxiv : the preprint server for biology·2026
Same author

Controlled intramural fluid injection to quantify propensity to thoracic aortic dissection.

Research square·2026
Same author

Postnatal pulmonary artery development from transcript to tissue.

Journal of the Royal Society, Interface·2026
Same author

Metabolic control of smooth muscle cell phenotype switching in atherosclerosis.

bioRxiv : the preprint server for biology·2026

Related Experiment Video

Updated: Oct 8, 2025

Precision Ultrasound-guided Stem Cell Delivery for Vascular Repair in Aortic Diseases
04:59

Precision Ultrasound-guided Stem Cell Delivery for Vascular Repair in Aortic Diseases

Published on: June 20, 2025

381

Progressive Microstructural Deterioration Dictates Evolving Biomechanical Dysfunction in the Marfan Aorta.

Cristina Cavinato1, Minghao Chen2, Dar Weiss1

  • 1Department of Biomedical Engineering, Yale University, New Haven, CT, United States.

Frontiers in Cardiovascular Medicine
|January 3, 2022
PubMed
Summary
This summary is machine-generated.

Marfan syndrome causes thoracic aortic aneurysms by damaging elastic fibers. This study links microstructural defects to mechanical changes, revealing how aortic functionality declines with disease progression.

Keywords:
Marfan syndromecollagenelastic fibersfibrillin-1stiffness

More Related Videos

Optical Coherence Tomography Based Biomechanical Fluid-Structure Interaction Analysis of Coronary Atherosclerosis Progression
13:07

Optical Coherence Tomography Based Biomechanical Fluid-Structure Interaction Analysis of Coronary Atherosclerosis Progression

Published on: January 15, 2022

4.1K
Imaging of the Microstructural Failure Mechanism in the Human Hip
08:43

Imaging of the Microstructural Failure Mechanism in the Human Hip

Published on: September 29, 2023

963

Related Experiment Videos

Last Updated: Oct 8, 2025

Precision Ultrasound-guided Stem Cell Delivery for Vascular Repair in Aortic Diseases
04:59

Precision Ultrasound-guided Stem Cell Delivery for Vascular Repair in Aortic Diseases

Published on: June 20, 2025

381
Optical Coherence Tomography Based Biomechanical Fluid-Structure Interaction Analysis of Coronary Atherosclerosis Progression
13:07

Optical Coherence Tomography Based Biomechanical Fluid-Structure Interaction Analysis of Coronary Atherosclerosis Progression

Published on: January 15, 2022

4.1K
Imaging of the Microstructural Failure Mechanism in the Human Hip
08:43

Imaging of the Microstructural Failure Mechanism in the Human Hip

Published on: September 29, 2023

963

Area of Science:

  • Cardiovascular Biology
  • Biomechanical Engineering
  • Genetics

Background:

  • Thoracic aortic aneurysms often result from fibrillin-1 gene mutations, leading to Marfan syndrome.
  • Fibrillin-1 is crucial for elastic fibers, essential for aortic wall structure and function.
  • Current understanding lacks a direct link between microstructural defects and mechanical properties in fibrillin-1 related aortopathies.

Purpose of the Study:

  • To correlate microstructural defects with mechanical property changes in the aorta during Marfan syndrome progression.
  • To investigate the impact of fibrillin-1 deficiency on aortic wall integrity and functionality.

Main Methods:

  • Utilized age-matched wild-type, Fbn1(mgR/mgR), and Fbn1(ln/ln) mouse models representing varying Marfan aortic phenotypes.
  • Performed ex vivo multiphoton imaging and biaxial mechanical testing on ascending and descending thoracic aortas.
  • Conducted 3D microstructural characterization under physiological loading.

Main Results:

  • Elastic fiber defects, collagen remodeling, and cell reorganization increase with aortic dilatation.
  • Medial degeneration patterns shift from radial to more uniform with increasing dilatation.
  • Aortic functionality declines, evidenced by increased circumferential material stiffness and reduced elastic energy storage.

Conclusions:

  • Microstructural degeneration in Marfan aortopathy directly correlates with altered biomechanical properties.
  • These changes compromise aortic functionality, with increasing stiffness and decreased energy storage.
  • The study provides a quantitative link between structural defects and mechanical decline in Marfan syndrome.