Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Regulation of Angiogenesis and Blood Supply

Regulation of Angiogenesis and Blood Supply

Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits. Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl hydroxylase and factor...

Acute Inflammation III: Local and Systemic Effects

Acute Inflammation III: Local and Systemic Effects

Acute inflammation produces a coordinated set of local and systemic changes that limit injury, eliminate pathogens, and initiate repair. These responses arise within minutes of infection, trauma, or chemical insult and are driven by vascular alterations and leukocyte-derived mediators. When the stimulus resolves, the reaction typically abates within days.Local EffectsAt the site of injury, arteriolar vasodilation increases blood flow, resulting in redness and warmth. Simultaneously, increased...

Vascular Spasm

Vascular Spasm

The vascular phase, also known as vasospasm, is the initial stage of hemostasis, crucial for preventing excessive bleeding when a blood vessel is injured. After a vessel is cut, nerves in the damaged area trigger pain and other sensory impulses. Simultaneously, the smooth muscles in the vessel wall contract, resulting in a vascular spasm. This contraction reduces the vessel's diameter at the injury site, slowing or stopping blood loss through the vessel wall. Vascular spasms typically last for...

Mechanism of Angiogenesis

Mechanism of Angiogenesis

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...

Inflammatory Response I: Vascular and Cellular

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,...

The Extracellular Matrix

The Extracellular Matrix

In order to maintain tissue organization, many animal cells are surrounded by structural molecules that make up the extracellular matrix (ECM). Together, the molecules in the ECM maintain the structural integrity of tissue as well as the remarkable specific properties of certain tissues.Composition of the Extracellular MatrixThe extracellular matrix (ECM) is commonly composed of ground substance, a gel-like fluid, fibrous components, and many structurally and functionally diverse molecules.

You might also read

Related Articles

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

Sort by

Same author

<i>Mir147</i> Limits the Contribution of Non-Foamy Macrophages to Atherosclerosis.

Circulation·2026

Same author

Impact of a Clinical Valve Coordinator on Hospital Length of Stay and Patient Outcomes: Results From the BENCHMARK Registry.

Structural heart : the journal of the Heart Team·2026

Same author

Biotechnical Multiscale Engineering of Scaffolds for Stem Cell and Organoid Research.

Small (Weinheim an der Bergstrasse, Germany)·2025

Same author

A comprehensive strategy for pandemic preparedness with neutralizing monoclonal antibodies.

mAbs·2025

Same author

Combination of 3D Micro Contact Printing and Scraping Technique for Site Selective Cocultivation Across a Porous Micro Structured Scaffold.

Small (Weinheim an der Bergstrasse, Germany)·2025

Same author

An interplay of non-coding RNAs regulates <i>CDH13</i> expression and affects endothelial function and coronary artery disease risk.

Research square·2025

Search research articles

Related Experiment Video

Updated: Jun 30, 2026

Murine Aortic Crush Injury: An Efficient In Vivo Model of Smooth Muscle Cell Proliferation and Endothelial Function

Murine Aortic Crush Injury: An Efficient In Vivo Model of Smooth Muscle Cell Proliferation and Endothelial Function

Published on: June 11, 2017

Chemokines in vascular dysfunction and remodeling.

Andreas Schober¹

¹Cardiology Unit, Medizinische Poliklinik, University of Munich, Medical Policlinic-City Center Campus, University of Munich, Munich, Germany. andreas.schober@med.uni-muenchen.de

Arteriosclerosis, Thrombosis, and Vascular Biology

|September 27, 2008

Summary

Vascular remodeling involves vessel wall changes, often leading to narrowed arteries. Specific chemokines drive this process, but some, like KC/Gro-alpha, promote healing and reduce narrowing.

More Related Videos

Development and Characterization of In Vitro Microvessel Network and Quantitative Measurements of Endothelial [Ca2+]i and Nitric Oxide Production

Development and Characterization of In Vitro Microvessel Network and Quantitative Measurements of Endothelial [Ca²⁺]_iand Nitric Oxide Production

Published on: May 19, 2016

Related Experiment Videos

Last Updated: Jun 30, 2026

Murine Aortic Crush Injury: An Efficient In Vivo Model of Smooth Muscle Cell Proliferation and Endothelial Function

Murine Aortic Crush Injury: An Efficient In Vivo Model of Smooth Muscle Cell Proliferation and Endothelial Function

Published on: June 11, 2017

Development and Characterization of In Vitro Microvessel Network and Quantitative Measurements of Endothelial [Ca2+]i and Nitric Oxide Production

Development and Characterization of In Vitro Microvessel Network and Quantitative Measurements of Endothelial [Ca²⁺]_iand Nitric Oxide Production

Published on: May 19, 2016

Area of Science:

Cardiovascular Biology
Immunology
Cell Biology

Background:

Vascular remodeling, characterized by vessel wall structural changes, can cause luminal narrowing and hypoperfusion.
Key events include smooth muscle cell (SMC) accumulation, inflammatory cell infiltration, and endothelial regeneration.
Chemokines and their receptors critically influence neointima formation and vascular repair.

Purpose of the Study:

To investigate the role of specific chemokine-chemokine receptor pairs in vascular remodeling.
To understand how chemokines regulate SMC accumulation, inflammatory cell infiltration, and endothelial repair.

Main Methods:

Analysis of chemokine and chemokine receptor involvement in vascular remodeling processes.
Examination of the impact of specific chemokine pathways on SMCs, leukocytes, and endothelial cells.

Main Results:

Stromal cell-derived factor-1alpha (SDF-1alpha) via CXCR4 promotes maladaptive SMC progenitor cell recruitment.
Monocyte chemoattractant protein-1 (MCP-1)/CCR2, RANTES/CCR5, and Fractalkine/CX(3)CR1 direct leukocyte infiltration and MCP-1/CCR2 and Fractalkine/CX(3)CR1 enhance SMC expansion.
Keratinocyte chemoattractant (KC)/Gro-alpha via CXCR2 supports endothelial recovery, attenuating neointima formation.

Conclusions:

The chemokine network plays a dual role in vascular remodeling, with some pathways promoting pathological changes and others facilitating repair.
Targeting specific chemokine functions offers a potential therapeutic strategy for obstructive vascular remodeling.
Understanding the distinct roles of chemokines like SDF-1alpha, MCP-1, RANTES, Fractalkine, and KC is crucial for therapeutic intervention.