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Related Concept Videos

Complement System01:27

Complement System

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 membrane...
Acute Inflammation III: Local and Systemic Effects01:25

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...
Introduction to Hemostasis01:05

Introduction to Hemostasis

Hemostasis is a complex physiological process that prevents excessive bleeding when a blood vessel is injured. It's crucial for maintaining the integrity of the circulatory system, as it ensures that our blood remains fluid while still within the vascular network and yet clots to prevent blood loss upon vessel injury.
The three phases of hemostasis involve many clotting factors present in plasma and several substances released by platelets and injured tissue cells. It is a fast, localized, and...
Antimicrobial Proteins01:23

Antimicrobial Proteins

Antimicrobial proteins are important components of the immune system. They aid the body in combating pathogens by either killing them directly or hindering their replication processes. Four main types of antimicrobial substances are interferons, the complement system, iron-binding proteins, and antimicrobial proteins.
Interferons
Interferons (IFNs) are proteins produced by lymphocytes, macrophages, and fibroblasts infected with viruses. While IFNs cannot prevent viruses from entering and...
Cellular Injury I: Introduction01:00

Cellular Injury I: Introduction

Cellular injury occurs when a cell cannot maintain homeostasis or adapt to stressors such as hypoxia, toxins, or trauma. Depending on severity and duration, injury may be reversible, allowing recovery, or irreversible, leading to cell death.General Mechanisms of Cell InjuryAlthough causes vary, most cellular injuries arise from a few key mechanisms that disrupt essential functions and often amplify one another. Cell survival depends on the extent and balance of these disturbances.ATP depletion...
Extrinsic and Intrinsic Pathways of Hemostasis01:20

Extrinsic and Intrinsic Pathways of Hemostasis

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 forms a...

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Related Experiment Video

Updated: May 18, 2026

Murine Model of Intestinal Ischemia-reperfusion Injury
07:07

Murine Model of Intestinal Ischemia-reperfusion Injury

Published on: May 11, 2016

The complement system in ischemia-reperfusion injuries.

William B Gorsuch1, Elvina Chrysanthou, Wilhelm J Schwaeble

  • 1Center for Experimental Therapeutics and Reperfusion Injury, Department of Anesthesiology, Perioperative and Pain Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.

Immunobiology
|September 12, 2012
PubMed
Summary

Ischemia and reperfusion injury involves tissue damage and inflammation. This review highlights activated complement pathways, involved components, and clinical inhibitors for ischemia/reperfusion injury, offering an updated view for future research.

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Area of Science:

  • Immunology
  • Pathophysiology
  • Pharmacology

Background:

  • Ischemia and reperfusion (I/R) injury is a significant clinical challenge across multiple organs.
  • The complement system plays a critical role in mediating inflammation and tissue damage following I/R events.
  • Extensive research has explored the involvement of complement in I/R injury over several decades.

Purpose of the Study:

  • To provide an updated overview of the complement system's role in ischemia/reperfusion (I/R) injury.
  • To detail the specific complement pathways and components activated during I/R.
  • To review current clinical biologics and inhibitors used in managing I/R.

Main Methods:

  • Literature review focusing on recent advancements in complement research related to I/R injury.
  • Analysis of activated complement pathways (classical, lectin, alternative) in the context of I/R.
  • Survey of clinically relevant complement inhibitors and their therapeutic potential.

Main Results:

  • Identification of key complement components (e.g., C3, C5a) central to I/R-induced inflammation.
  • Overview of how different complement pathways contribute uniquely to I/R pathophysiology.
  • Summary of the efficacy and limitations of existing complement-targeting biologics in clinical settings.

Conclusions:

  • The complement system is a pivotal mediator of I/R injury, presenting therapeutic targets.
  • Clinical application of complement inhibitors offers a promising strategy for mitigating I/R damage.
  • Further research is essential to optimize complement-targeted therapies and fully understand their clinical utility.