Related Experiment Video

Updated: Jul 18, 2026

Cecal Ligation Puncture Procedure
11:53

Cecal Ligation Puncture Procedure

Published on: May 7, 2011

Activated protein C in sepsis and beyond: update 2006

Lisa J Toltl1, Lucy Y Y Shin, Patricia C Y Liaw

  • 1Department of Medical Sciences at McMaster University, and the Henderson Research Centre, Hamilton, Ontario, Canada.

Insights

Activated protein C (APC) is an anticoagulant that also acts as a signaling molecule. Research shows APC has therapeutic potential beyond sepsis, including in stroke and wound healing.

Area of Science:

  • Biochemistry
  • Physiology
  • Pharmacology

Background:

  • Activated protein C (APC) is a plasma serine protease primarily known for its anticoagulant properties.
  • APC degrades coagulation factors Va and VIIIa, inhibiting the coagulation cascade.
  • Recent research reveals APC as a signaling molecule linking coagulation, inflammation, apoptosis, and vascular permeability.

Purpose of the Study:

  • To review key studies on the diverse biological activities of APC.
  • To summarize the therapeutic potential of APC beyond its anticoagulant function.
  • To explore APC's role in conditions such as sepsis, stroke, and wound healing.

Main Methods:

  • Comprehensive literature review of PubMed up to May 2006.
  • Analysis of studies investigating APC's anticoagulant and signaling functions.
  • Synthesis of research on APC's therapeutic applications in various diseases.

Main Results:

  • APC exhibits multifaceted biological activities beyond anticoagulation.
  • APC modulates pathways involved in sepsis, inflammation, and cell death.
  • Evidence supports APC's therapeutic potential in stroke, ischemia-reperfusion injury, and wound healing.

Conclusions:

  • APC is a critical signaling molecule with broad therapeutic implications.
  • APC's protective effects in sepsis are linked to its ability to modulate multiple pathways.
  • Further research into APC's non-anticoagulant functions may unlock new treatment strategies.

Related Concept Videos

Acute Kidney Injury II: Pathophysiology01:29

Acute Kidney Injury II: Pathophysiology

Acute kidney injury (AKI) causes are categorized into three primary categories based on the location of the injury: prerenal, intrarenal (or intrinsic), and postrenal causes. This classification guides clinical management and illustrates how different pathways can impair kidney function.Etiology and Pathophysiology of Acute Kidney Injury1. Prerenal causesEtiology: Prerenal Acute Kidney Injury, the most common type, occurs when reduced blood flow to the kidneys decreases filtration capacity...
Acute Kidney Injury IV: Diagnostic Studies and Prevention01:30

Acute Kidney Injury IV: Diagnostic Studies and Prevention

Accurate diagnosis and effective prevention are critical in managing Acute Kidney Injury (AKI), which is linked to high mortality rates ranging from 10% to 80%. Timely recognition of at-risk patients and careful monitoring can significantly reduce the likelihood of kidney damage.Diagnostic Assessments:The diagnostic process starts with a comprehensive medical history to identify prerenal, intrarenal, and postrenal causes.Prerenal causes, such as dehydration, hypotension, or blood loss, should...
Acute Kidney Injury I: Introduction01:22

Acute Kidney Injury I: Introduction

Introduction:Acute Kidney Injury (AKI) describes a swift decrease in kidney function occurring over hours to days, characterized by the kidneys' failure to remove waste products from the bloodstream. This leads to dangerous complications like metabolic acidosis, fluid overload, and electrolyte imbalances, such as hyperkalemia, which can cause life-threatening arrhythmias. AKI is common in both hospital and outpatient settings, often triggered by dehydration, sepsis, or exposure to nephrotoxic...
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...
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 Kidney Injury III: Clinical Manifestations01:29

Acute Kidney Injury III: Clinical Manifestations

Acute Kidney Injury (AKI) progresses through distinct clinical phases: the oliguric, diuretic, and recovery phases, each marked by unique manifestations and challenges.Oliguric Phase:The oliguric phase is the initial stage of AKI, typically lasting 10 to 14 days. This phase is marked by a significant reduction in urine output, usually less than 400 mL per day, indicating decreased kidney function. Fluid retention is a prominent feature, leading to symptoms such as edema, hypertension, and...