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

Peripheral Artery Disease I: Introduction01:30

Peripheral Artery Disease I: Introduction

Peripheral artery disease (PAD) predominantly results from atherosclerosis, which involves the accumulation of fatty deposits, or plaques, within the walls of arteries. This causes them to narrow and harden, significantly reducing blood flow. PAD predominantly affects the legs, particularly the arteries supplying the thighs and calves. In rare cases, it may involve other arteries, including those in the arms.Etiology of PAD:The principal cause of PAD is atherosclerosis, which results from fatty...
Coronary Artery Disease II: Pathophysiology01:26

Coronary Artery Disease II: Pathophysiology

Coronary Artery Disease (CAD) originates from a series of events that impair the function of coronary arteries, the blood vessels responsible for delivering oxygen-rich blood to the heart muscle. The pathophysiology of CAD is closely linked to atherosclerosis, a chronic inflammatory and lipid-driven condition affecting the vascular endothelium.1. Endothelial DamageThe process begins with damage to the vascular endothelium, which serves as a protective barrier between the blood and the vessel...
Atherosclerosis I: Introduction01:30

Atherosclerosis I: Introduction

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...
Aneurysm I: Introduction01:30

Aneurysm I: Introduction

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...
Pulmonary Hypertension: Classification and Pathogenesis01:30

Pulmonary Hypertension: Classification and Pathogenesis

Pulmonary hypertension (PH) is a severe health condition in which the mean pulmonary arterial pressure increases to 25 mmHg or more, even when the body is at rest. This high pressure in the blood vessels that transport blood from the heart to the lungs can cause various symptoms, including shortness of breath, can lead to right heart failure, and significantly affect the overall quality of life.
There are various classifications for PH, each relating to different underlying causes and also...
Coronary Artery Disease I: Introduction01:30

Coronary Artery Disease I: Introduction

Coronary Artery Disease (CAD): An Overview with Scientific InsightsCoronary Artery Disease (CAD), often referred to as C-A-D, is a prevalent blood vessel disorder classified under the broader category of atherosclerosis. Atherosclerosis is a pathological process characterized by the hardening and narrowing of arteries due to the accumulation of atherosclerotic plaques. These plaques are composed of cholesterol, fatty substances, inflammatory cells, calcium, and fibrin, reducing blood flow to...

You might also read

Related Articles

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

Sort by
Same author

Local hemodynamic changes and branch outcomes associated with inner branched versus outer branched stent grafts.

Annals of vascular surgery·2026
Same author

Comparison of endovascular procedures of the lower extremities and iliac arteries with and without navigation assistance Vascular Navigation PAD: study protocol for a prospective multicenter randomized clinical trial.

Trials·2026
Same author

Interdisciplinary vascular genetics evaluations in routine clinical care: insights from a five-year single-center experience.

Langenbeck's archives of surgery·2026
Same author

HYPOChLorous Acid TEsting Studies in elective groin VASCULAR surgery (HYPOCLATES:VASCULAR): protocol for an ambispective cohort study evaluating a standard change to hypochlorous acid lavage in patients undergoing elective groin vascular surgery.

BMC surgery·2026
Same author

State-of-the-Art Definitive Femoropopliteal Lesion Treatment: A Case-Based Systematic Approach.

Journal of cardiovascular development and disease·2026
Same author

Reply.

Journal of vascular surgery·2026

Related Experiment Video

Updated: Jun 16, 2026

Murine Model of Thoracic Aortic Dissection Induced by Oral β-Aminopropionitrile and Subcutaneous Angiotensin II Infusion
05:31

Murine Model of Thoracic Aortic Dissection Induced by Oral β-Aminopropionitrile and Subcutaneous Angiotensin II Infusion

Published on: May 16, 2025

Spontaneous arterial dissection: phenotype and molecular pathogenesis.

Caspar Grond-Ginsbach1, Rastislav Pjontek, Suna Su Aksay

  • 1Department of Neurology, University of Heidelberg, Heidelberg, Germany. Caspar.Grond-Ginsbach@med.uni-heidelberg.de

Cellular and Molecular Life Sciences : CMLS
|February 16, 2010
PubMed
Summary

Arterial dissection (AD) involves splitting of the arterial wall due to bleeding, characterized by medial degeneration. Genetic factors affecting extracellular matrix, TGF-beta signaling, and smooth muscle cells are implicated in AD development.

More Related Videos

Investigating the Pathogenesis of MYH7 Mutation Gly823Glu in Familial Hypertrophic Cardiomyopathy using a Mouse Model
03:45

Investigating the Pathogenesis of MYH7 Mutation Gly823Glu in Familial Hypertrophic Cardiomyopathy using a Mouse Model

Published on: August 8, 2022

Related Experiment Videos

Last Updated: Jun 16, 2026

Murine Model of Thoracic Aortic Dissection Induced by Oral β-Aminopropionitrile and Subcutaneous Angiotensin II Infusion
05:31

Murine Model of Thoracic Aortic Dissection Induced by Oral β-Aminopropionitrile and Subcutaneous Angiotensin II Infusion

Published on: May 16, 2025

Investigating the Pathogenesis of MYH7 Mutation Gly823Glu in Familial Hypertrophic Cardiomyopathy using a Mouse Model
03:45

Investigating the Pathogenesis of MYH7 Mutation Gly823Glu in Familial Hypertrophic Cardiomyopathy using a Mouse Model

Published on: August 8, 2022

Area of Science:

  • Cardiovascular Biology
  • Genetics
  • Pathology

Background:

  • Arterial dissection (AD) is a serious condition involving arterial wall splitting from intramural bleeding.
  • It can spontaneously affect various arteries and is histologically marked by medial degeneration.
  • Medial degeneration disrupts key cellular processes like inflammation, proteolysis, and smooth muscle cell function.

Purpose of the Study:

  • To investigate the underlying biological processes and genetic factors contributing to arterial dissection.
  • To identify specific genes and pathways involved in the pathogenesis of medial degeneration.
  • To explore the genetic basis of spontaneous arterial dissection.

Main Methods:

  • Histological examination of affected arteries.
  • Gene expression profiling and proteome studies.
  • Genetic linkage analysis and genome-wide association studies (GWAS).

Main Results:

  • Disturbances in inflammation, proteolytic activity, cell proliferation, apoptosis, and smooth muscle cell (SMC) contractile function were observed.
  • Mutations in genes related to extracellular matrix (FBN1, COL3A1), TGF-beta signaling (FBN1, TGFBR1, TGFBR2), and SMC contractile system (ACTA2, MYH11) were identified.
  • The CDKN2A/CDKN2B locus was suggested to play a role in AD etiology.

Conclusions:

  • Arterial dissection is linked to complex molecular and genetic alterations in the arterial wall.
  • Rare Mendelian disorders affecting extracellular matrix, TGF-beta signaling, and SMCs are significant causes of AD.
  • Further research into genetic loci like CDKN2A/CDKN2B may elucidate AD pathogenesis.