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

Atherosclerosis I: Introduction01:30

Atherosclerosis I: Introduction

718
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...
718
Mitral Stenosis I: Introduction01:22

Mitral Stenosis I: Introduction

350
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...
350
Peripheral Artery Disease I: Introduction01:30

Peripheral Artery Disease I: Introduction

268
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...
268
Myocarditis I: Introduction01:21

Myocarditis I: Introduction

311
Myocarditis is inflammation of the myocardium, which is the muscular layer of the heart.EtiologyMyocarditis has a diverse etiology, including a wide range of infectious and non-infectious causes:Infectious CausesViral: Common viruses include Coxsackie A and B, adenovirus, parvovirus B19, enteroviruses, and influenza A.Bacterial: Examples include infections caused by Streptococcus, Staphylococcus, and Mycoplasma species.Rickettsial: Infections like Rocky Mountain spotted fever can result in...
311
Mechanism of Angiogenesis01:10

Mechanism of Angiogenesis

6.5K
Blood vessel formation starts early during embryonic development, around day 7. In the extraembryonic yolk sac, mesodermal precursor cells called hemangioblast proliferate and differentiate into angioblast. Angioblasts express vascular endothelial growth factor receptor 2 or VEGFR2, which binds VEGF-A, a proangiogenic factor, guiding blood vessel formation. VEGF signaling promotes angioblasts to form a blood island in the developing embryo. Angioblasts further differentiate, giving rise to...
6.5K
Coronary Artery Disease II: Pathophysiology01:26

Coronary Artery Disease II: Pathophysiology

322
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...
322

You might also read

Related Articles

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

Sort by
Same author

Nonlinear Measures Applied to Spontaneous Infant Movement Analysis: A Scoping Review.

Sensors (Basel, Switzerland)·2026
Same author

NLRP3 Inflammasome and IL-1-Mediated Inflammation in Human Carotid Atherosclerosis: A Systematic Review of Endarterectomy-Based Evidence.

Medical sciences (Basel, Switzerland)·2026
Same author

HHC-induced psychosis in adolescents: a case series.

Irish journal of psychological medicine·2026
Same author

Endovenous ablation of the great saphenous varicose veins: Does the modality matter? A prospective cohort study.

Phlebology·2026
Same author

Functionalized smart surfaces to control the wound healing after glaucoma's surgery.

International journal of pharmaceutics·2026
Same author

Mutual Influence of Sucralose and Bisphenol A on Biological and Neurobehavioral Action in <i>Drosophila melanogaster</i>.

International journal of molecular sciences·2026

Related Experiment Video

Updated: Jan 3, 2026

A Rat Carotid Artery Pressure-Controlled Segmental Balloon Injury with Periadventitial Therapeutic Application
06:53

A Rat Carotid Artery Pressure-Controlled Segmental Balloon Injury with Periadventitial Therapeutic Application

Published on: July 9, 2020

5.4K

Neointimal Hyperplasia.

Sandra Figueiredo Braga1, João Rocha Neves2, Joana Ferreira1

  • 1Serviço de Angiologia e Cirurgia Vascular, Hospital da Senhora da Oliveira, EPE, Guimarães, Portugal.

Revista Portuguesa De Cirurgia Cardio-Toracica E Vascular : Orgao Oficial Da Sociedade Portuguesa De Cirurgia Cardio-Toracica E Vascular
|November 18, 2019
PubMed
Summary

Neointimal hyperplasia, a vessel repair response, involves complex cellular processes. Understanding its pathophysiology and risk factors aids in developing prevention and treatment strategies.

More Related Videos

Development of a Murine Model for Femoral Artery Anastomotic Stenosis
05:42

Development of a Murine Model for Femoral Artery Anastomotic Stenosis

Published on: April 18, 2025

568
Balloon-based Injury to Induce Myointimal Hyperplasia in the Mouse Abdominal Aorta
07:32

Balloon-based Injury to Induce Myointimal Hyperplasia in the Mouse Abdominal Aorta

Published on: February 7, 2018

10.0K

Related Experiment Videos

Last Updated: Jan 3, 2026

A Rat Carotid Artery Pressure-Controlled Segmental Balloon Injury with Periadventitial Therapeutic Application
06:53

A Rat Carotid Artery Pressure-Controlled Segmental Balloon Injury with Periadventitial Therapeutic Application

Published on: July 9, 2020

5.4K
Development of a Murine Model for Femoral Artery Anastomotic Stenosis
05:42

Development of a Murine Model for Femoral Artery Anastomotic Stenosis

Published on: April 18, 2025

568
Balloon-based Injury to Induce Myointimal Hyperplasia in the Mouse Abdominal Aorta
07:32

Balloon-based Injury to Induce Myointimal Hyperplasia in the Mouse Abdominal Aorta

Published on: February 7, 2018

10.0K

Area of Science:

  • Vascular Biology
  • Pathophysiology
  • Biomedical Engineering

Background:

  • Neointimal hyperplasia is a physiological healing response to vascular injury.
  • This complex process involves multiple cell types and signaling pathways across arterial layers.
  • Risk factors include diabetes, systemic inflammation, and material properties of endovascular/surgical interventions.

Purpose of the Study:

  • To discuss the pathophysiology of neointimal hyperplasia.
  • To explore strategies for the prevention and treatment of neointimal hyperplasia.

Main Methods:

  • Review of existing literature on neointimal hyperplasia.
  • Analysis of cellular and molecular mechanisms involved in the healing response.
  • Identification of known risk factors and their impact.

Main Results:

  • Neointimal hyperplasia is a multifactorial process with numerous potential therapeutic targets.
  • Identified risk factors contribute significantly to the development and severity of neointimal hyperplasia.
  • Understanding the complex interplay of factors is crucial for effective intervention.

Conclusions:

  • Targeting specific molecular pathways and addressing risk factors can inhibit neointimal hyperplasia.
  • Further research into prevention and treatment strategies is warranted.
  • Comprehensive understanding of pathophysiology is key to managing vascular healing responses.