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

Chronic Inflammation: Introduction01:12

Chronic Inflammation: Introduction

Chronic inflammation is a prolonged, dysregulated immune response that persists for weeks to years when the inciting stimulus is difficult to eradicate or when self‑antigens drive ongoing reactivity. Morphologically, it is defined by mononuclear cell infiltration, progressive tissue destruction, and concurrent attempts at healing via angiogenesis and fibrosis. Compared with acute inflammation, edema is less prominent while cellular infiltration predominates; triggers include persistent...
Inflammation01:38

Inflammation

Overview
Inflammatory Response I: Vascular and Cellular01:30

Inflammatory Response I: Vascular and Cellular

The inflammatory response is the body's defense against infection, injury, or irritation from bacteria, trauma, toxins, or heat. Inflammation helps locate and destroy pathogens and remove damaged tissue elements to heal the body. During this initial phase, fluid, blood products, and nutrients migrate to the injured area, resulting in redness, heat, swelling, ache, and loss of function. Moreover, signs of systemic inflammation include fever, increased WBC count, malaise, anorexia, nausea,...
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...

You might also read

Related Articles

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

Sort by
Same author

Cardiac Pacemaker Cells Harness Stochastic Resonance to Avoid Sinus Arrest.

Circulation research·2026
Same author

Emergence of heartbeat frailty in advanced age II: individual cardiovascular aging trajectories revealed by lifelong echocardiography in male mice.

GeroScience·2026
Same author

cAMP-Activated EPAC Signaling Is an Integral Component of Cardiac Pacemaker Cell Automaticity.

Circulation. Arrhythmia and electrophysiology·2026
Same author

Cardiac Pacemaker Cells Harness Stochastic Resonance to Ensure Fail-Safe Operation at Low Rates Bordering on Sinus Arrest.

bioRxiv : the preprint server for biology·2026
Same author

A new Fight-or-Flight Pacemaker Mechanism via Ryanodine Receptor abundance and superclustering.

PLoS computational biology·2026
Same author

Glucose-6-Phosphate Dehydrogenase Modifies the Impact of Glucose on Arterial Aging in A Sex-Specific Manner.

Journal of the American Heart Association·2026

Related Experiment Video

Updated: Jul 15, 2026

Quantitative Analysis and Characterization of Atherosclerotic Lesions in the Murine Aortic Sinus
06:43

Quantitative Analysis and Characterization of Atherosclerotic Lesions in the Murine Aortic Sinus

Published on: December 7, 2013

Proinflammatory profile within the grossly normal aged human aortic wall.

Mingyi Wang1, Jing Zhang, Li-Qun Jiang

  • 1National Institute on Aging, National Institutes of Health, Baltimore, MD 21224-6825, USA. mingyiw@grc.nia.nih.gov

Hypertension (Dallas, Tex. : 1979)
|April 25, 2007
PubMed
Summary

Aging human aortas show increased inflammation and smooth muscle cell invasion, driven by angiotensin II signaling. These age-related changes create a substrate for arterial diseases like atherosclerosis and hypertension.

More Related Videos

Flow Cytometry Analysis of Immune Cells Within Murine Aortas
15:15

Flow Cytometry Analysis of Immune Cells Within Murine Aortas

Published on: July 1, 2011

Related Experiment Videos

Last Updated: Jul 15, 2026

Quantitative Analysis and Characterization of Atherosclerotic Lesions in the Murine Aortic Sinus
06:43

Quantitative Analysis and Characterization of Atherosclerotic Lesions in the Murine Aortic Sinus

Published on: December 7, 2013

Flow Cytometry Analysis of Immune Cells Within Murine Aortas
15:15

Flow Cytometry Analysis of Immune Cells Within Murine Aortas

Published on: July 1, 2011

Area of Science:

  • Cardiovascular Science
  • Aging Research
  • Vascular Biology

Background:

  • Animal studies suggest aging increases angiotensin II and related molecules in arteries.
  • It remains unknown if these age-related changes occur in the human arterial wall.

Purpose of the Study:

  • To investigate age-related changes in the human thoracic aorta.
  • To determine if inflammation and smooth muscle cell characteristics change with age in normal aortas.

Main Methods:

  • Human thoracic aortas from young and old males were analyzed post-necropsy.
  • Levels of angiotensin II, matrix metalloproteinases (MMPs), monocyte chemoattractant protein-1 (MCP-1), and collagen were quantified.
  • Smooth muscle cell invasion assays and cell phenotyping were performed.

Main Results:

  • Older aortas exhibited thickened intima with increased angiotensin-converting enzyme, angiotensin II, angiotensin II receptor type 1, MMPs 2/9, MCP-1, and collagen I/III.
  • In situ MMP activity and the presence of fetal-type smooth muscle cells were higher in older aortas.
  • Age-related increases in smooth muscle cell invasiveness were observed, exacerbated by angiotensin II and mitigated by MMP or angiotensin II receptor blockers.

Conclusions:

  • The aged human aorta, even without lipid infiltration, displays a pro-inflammatory profile.
  • Increased angiotensin II signaling, MMP activity, and smooth muscle cell plasticity contribute to age-related aortic wall changes.
  • These alterations create a favorable environment for the development of atherosclerosis and hypertension.