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

Inflammation01:38

Inflammation

59.5K
Overview
59.5K
Peripheral Artery Disease I: Introduction01:30

Peripheral Artery Disease I: Introduction

188
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...
188
Atherosclerosis I: Introduction01:30

Atherosclerosis I: Introduction

528
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...
528
Chronic Obstructive Pulmonary Disease-II: Pathophysiology01:20

Chronic Obstructive Pulmonary Disease-II: Pathophysiology

3.9K
Chronic Obstructive Pulmonary Disease (COPD) pathophysiology is intricate and multifaceted, involving a complex interplay of physiological processes. Understanding these mechanisms is crucial for effectively managing and treating COPD. Here is an in-depth look at the critical elements in the pathophysiology of COPD:
Chronic Inflammation
3.9K
Coronary Artery Disease II: Pathophysiology01:26

Coronary Artery Disease II: Pathophysiology

230
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...
230
Inflammatory Response I: Vascular and Cellular01:30

Inflammatory Response I: Vascular and Cellular

14.8K
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,...
14.8K

You might also read

Related Articles

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

Sort by
Same author

Loss of NRF2 During Aging Contributes to Myocardial Functional Decline.

Antioxidants (Basel, Switzerland)·2026
Same author

Angiotensin II, miR-34a, and AGTRAP crosstalk in arterial smooth muscle cells.

GeroScience·2025
Same author

Unraveling Elastic Fiber-Derived Signaling in Arterial Aging and Related Arterial Diseases.

Biomolecules·2025
Same author

Enhanced vasorin signaling mitigates adverse cardiovascular remodeling.

Aging medicine (Milton (N.S.W))·2024
Same author

The Senescent Heart-"Age Doth Wither Its Infinite Variety".

International journal of molecular sciences·2024
Same author

Milk Fat Globule Epidermal Growth Factor VIII Fragment Medin in Age-Associated Arterial Adverse Remodeling and Arterial Disease.

Cells·2023
Same journal

Early Outcomes After Total Arch Replacement With Frozen Elephant Trunk in Elderly Patients With Acute Type A Aortic Dissection.

Aging medicine (Milton (N.S.W))·2026
Same journal

The Role of Artificial Intelligence in Medication Management for Older Adults: A Systematic Review.

Aging medicine (Milton (N.S.W))·2026
Same journal

Interpretation of A Focus Shift From Sarcopenia to Muscle Health in the Asian Working Group for Sarcopenia 2025 Consensus Update.

Aging medicine (Milton (N.S.W))·2026
Same journal

Reduced CB1 Cannabinoid Receptor Expression in Alzheimer's Disease and Transgenic Mouse Models.

Aging medicine (Milton (N.S.W))·2026
Same journal

The Role of Extracellular Vesicles MicroRNAs in Sarcopenia: From Aging to Multi-Morbidity.

Aging medicine (Milton (N.S.W))·2026
Same journal

Gender Disparities in the Prevalence, Trends, and Determinants of Later-Life Urinary Incontinence: A Disproportionate Burden on Women.

Aging medicine (Milton (N.S.W))·2026
See all related articles

Related Experiment Video

Updated: Dec 3, 2025

Measuring the Stiffness of Ex Vivo Mouse Aortas Using Atomic Force Microscopy
10:35

Measuring the Stiffness of Ex Vivo Mouse Aortas Using Atomic Force Microscopy

Published on: October 19, 2016

11.0K

Proinflammation, profibrosis, and arterial aging.

Mingyi Wang1, Robert E Monticone1, Kimberly R McGraw1

  • 1Laboratory of Cardiovascular Science National Institute on Aging National Institutes of Health Baltimore Maryland.

Aging Medicine (Milton (N.S.W))
|October 26, 2020
PubMed
Summary
This summary is machine-generated.

Aging causes arterial stiffening through a process called proinflammatory-profibrosis coupling. This involves increased collagen in blood vessels, driven by inflammation and specific molecular signals, leading to cardiovascular disease risk.

Keywords:
agingarterycollagenprofibrosisproinflammationstiffening

More Related Videos

Measuring Ascending Aortic Stiffness In Vivo in Mice Using Ultrasound
10:08

Measuring Ascending Aortic Stiffness In Vivo in Mice Using Ultrasound

Published on: December 2, 2014

16.3K
Assessment of Vascular Tone Responsiveness using Isolated Mesenteric Arteries with a Focus on Modulation by Perivascular Adipose Tissues
08:41

Assessment of Vascular Tone Responsiveness using Isolated Mesenteric Arteries with a Focus on Modulation by Perivascular Adipose Tissues

Published on: June 3, 2019

10.2K

Related Experiment Videos

Last Updated: Dec 3, 2025

Measuring the Stiffness of Ex Vivo Mouse Aortas Using Atomic Force Microscopy
10:35

Measuring the Stiffness of Ex Vivo Mouse Aortas Using Atomic Force Microscopy

Published on: October 19, 2016

11.0K
Measuring Ascending Aortic Stiffness In Vivo in Mice Using Ultrasound
10:08

Measuring Ascending Aortic Stiffness In Vivo in Mice Using Ultrasound

Published on: December 2, 2014

16.3K
Assessment of Vascular Tone Responsiveness using Isolated Mesenteric Arteries with a Focus on Modulation by Perivascular Adipose Tissues
08:41

Assessment of Vascular Tone Responsiveness using Isolated Mesenteric Arteries with a Focus on Modulation by Perivascular Adipose Tissues

Published on: June 3, 2019

10.2K

Area of Science:

  • Cardiovascular Biology
  • Aging Research
  • Vascular Medicine

Background:

  • Aging is a primary risk factor for cardiovascular diseases, strongly linked to arterial inflammation.
  • Age-related changes in arterial collagen, including cross-linking and degradation, are consequences of inflammation.
  • Vascular smooth muscle cells (VSMCs) in aging arteries produce increased collagen (types I, II, III) due to pro-inflammatory signaling, promoting fibrosis.

Purpose of the Study:

  • To elucidate the molecular mechanisms linking aging, inflammation, and arterial stiffening.
  • To investigate the role of specific signaling pathways in age-related arterial fibrosis.
  • To identify potential therapeutic targets for preventing age-associated arterial stiffening.

Main Methods:

  • Analysis of age-related changes in arterial collagen content, distribution, and properties.
  • Investigation of the role of pro-inflammatory molecules (angiotensin II, MFG-EGF-VIII, TGF-β1) and vasorin signaling.
  • Assessment of matrix metalloproteinase type II (MMP-2) activity and its interaction with TGF-β1.
  • Evaluation of the effects of blocking pro-inflammatory signaling pathways on arterial fibrosis and stiffening.

Main Results:

  • Aging arteries exhibit increased collagen deposition, primarily types I, II, and III, produced by stiffened VSMCs.
  • Pro-inflammatory signaling, involving angiotensin II, MFG-EGF-VIII, and TGF-β1, upregulates fibrosis, while vasorin signaling decreases.
  • Activated MMP-2 cleaves latent TGF-β, enhancing TGF-β1 activity and collagen accumulation.
  • Blocking pro-inflammatory pathways reduces fibrosis and prevents age-related arterial stiffening.

Conclusions:

  • The coupling of inflammation and fibrosis (proinflammatory-profibrosis) is the core mechanism behind age-related arterial stiffening.
  • Targeting pro-inflammatory signaling pathways offers a potential strategy to mitigate arterial stiffening and associated cardiovascular risks in aging individuals.