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

52.1K
Overview
52.1K
Complement System01:27

Complement System

2.0K
The complement system is a group of approximately 20 plasma proteins that strengthen the body's defenses against infections through opsonization, inflammation, and cell lysis. Opsonization involves coating pathogens with complement proteins, making them more recognizable and facilitating phagocyte engulfment. Certain complement proteins induce inflammation that attracts immune cells to the site of infection. Cell lysis involves the destruction of pathogens through the formation of a...
2.0K
Extrinsic and Intrinsic Pathways of Hemostasis01:20

Extrinsic and Intrinsic Pathways of Hemostasis

4.4K
Blood clotting or coagulation involves extrinsic and intrinsic pathways, which ultimately merge into the common pathway, forming a fibrin clot.
The Extrinsic Pathway
The extrinsic pathway of coagulation is typically initiated by tissue damage that exposes blood to tissue factor (TF), a protein released by the damaged tissue cells outside the blood vessels—this interaction with TF triggers biochemical reactions involving specific clotting factors. The key player here is Factor VII, which...
4.4K
Clot Retraction and Fibrinolysis01:16

Clot Retraction and Fibrinolysis

3.1K
After a fibrin clot is formed, the next step is clot retraction, a vital process facilitated by platelet contractile proteins, such as actin and myosin. These proteins pull the fibrin strands closer together and condense the clot. This action reduces the size of the clot, creating a smaller, denser structure that effectively seals off the damaged vessel. Clot retraction consolidates the clot and helps with wound healing by bringing the edges of the damaged blood vessel closer together.
3.1K
Formation of the Platelet Plug01:22

Formation of the Platelet Plug

3.5K
The platelet phase, the second stage of hemostasis, commences around 15-20 seconds after an injury. It follows and overlaps with the vascular phase, during which blood vessels constrict to minimize blood loss.
As the injured blood vessel contracts, endothelial cells undergo contraction, revealing collagen fibers in the basement membrane and underlying connective tissue. Furthermore, the plasma membrane of endothelial cells becomes adhesive, preparing the site for platelet adhesion. Platelets...
3.5K
Chronic Obstructive Pulmonary Disease-II: Pathophysiology01:20

Chronic Obstructive Pulmonary Disease-II: Pathophysiology

2.7K
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
2.7K

You might also read

Related Articles

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

Sort by
Same author

Coronary microvascular dysfunction: From diagnosis to therapy.

American journal of physiology. Heart and circulatory physiology·2026
Same author

Beta-Blockers After Myocardial Infarction With Preserved and Mildly Reduced Ejection Fraction: A Meta-Analysis With Trial Sequential Analysis.

European journal of clinical investigation·2026
Same author

Subcutaneous Adipose Tissue as a Metabolic Mirror: Transcriptomic Insights Into Glycaemic Dysregulation.

European journal of clinical investigation·2026
Same author

Aging in Focus: A Comprehensive View for Enhancing Healthspan.

European journal of clinical investigation·2026
Same author

GLP-1 receptor agonists and atherosclerosis: a metabolic treatment for a cardiometabolic disease.

European heart journal·2026
Same author

From biology to imaging: Rethinking vulnerable plaques in coronary artery disease.

European journal of clinical investigation·2026

Related Experiment Video

Updated: May 21, 2025

A Human Ex Vivo Atherosclerotic Plaque Model to Study Lesion Biology
05:51

A Human Ex Vivo Atherosclerotic Plaque Model to Study Lesion Biology

Published on: May 6, 2014

13.0K

Inflammation-Driven Plaque Erosion in Atherosclerosis: A Focus on Complement System Pathways.

Davide Ramoni1, Federico Carbone1,2, Simon Kraler3,4

  • 1Department of Internal Medicine, University of Genoa, 6 Viale Benedetto XV, 16132, Genoa, Italy.

Current Atherosclerosis Reports
|March 22, 2025
PubMed
Summary
This summary is machine-generated.

Complement system activation plays a key role in atherosclerosis development and progression. Ongoing research explores its dual role and therapeutic targeting to combat cardiovascular disease.

Keywords:
Anti-Complement TherapiesAtherosclerosisCardiovascular diseasesComplement systemInflammagingPlaque erosion

More Related Videos

Quantification of Monocyte Transmigration and Foam Cell Formation from Individuals with Chronic Inflammatory Conditions
09:41

Quantification of Monocyte Transmigration and Foam Cell Formation from Individuals with Chronic Inflammatory Conditions

Published on: October 17, 2017

13.3K
Induction of Atherosclerotic Plaques Through Activation of Mineralocorticoid Receptors in Apolipoprotein E-deficient Mice
07:36

Induction of Atherosclerotic Plaques Through Activation of Mineralocorticoid Receptors in Apolipoprotein E-deficient Mice

Published on: September 26, 2018

9.9K

Related Experiment Videos

Last Updated: May 21, 2025

A Human Ex Vivo Atherosclerotic Plaque Model to Study Lesion Biology
05:51

A Human Ex Vivo Atherosclerotic Plaque Model to Study Lesion Biology

Published on: May 6, 2014

13.0K
Quantification of Monocyte Transmigration and Foam Cell Formation from Individuals with Chronic Inflammatory Conditions
09:41

Quantification of Monocyte Transmigration and Foam Cell Formation from Individuals with Chronic Inflammatory Conditions

Published on: October 17, 2017

13.3K
Induction of Atherosclerotic Plaques Through Activation of Mineralocorticoid Receptors in Apolipoprotein E-deficient Mice
07:36

Induction of Atherosclerotic Plaques Through Activation of Mineralocorticoid Receptors in Apolipoprotein E-deficient Mice

Published on: September 26, 2018

9.9K

Area of Science:

  • Cardiovascular Science
  • Immunology
  • Molecular Biology

Background:

  • Complement system activation is increasingly recognized in atherogenesis.
  • It influences fatty streak formation, plaque destabilization, and thrombus formation.
  • Clinical sequelae include myocardial infarction, stroke, and premature death.

Purpose of the Study:

  • To review recent studies on complement activation in atherosclerotic plaque initiation and progression.
  • To explore the complex role of complement pathways in atherogenesis.
  • To discuss ongoing debates and therapeutic strategies targeting the complement cascade.

Main Methods:

  • Literature review of recent studies.
  • Analysis of complement components' interactions with cellular components of atherosclerotic plaques.
  • Examination of therapeutic approaches targeting the complement cascade.

Main Results:

  • Complement pathways modulate inflammatory processes, impacting plaque stability and healing.
  • Specific complement components (C3, C5b-9) accelerate atherosclerosis via cellular interactions.
  • The precise beneficial versus deleterious effects of complement activation remain debated.
  • Therapies targeting the complement cascade are under investigation to reduce plaque erosion and rupture.

Conclusions:

  • Complement activation is a significant factor in atherosclerosis, with complex and debated roles.
  • Modulating the complement cascade presents a potential therapeutic strategy for atherosclerotic cardiovascular disease.
  • Further research is needed to fully elucidate and leverage complement's role in cardiovascular health.