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Related Concept Videos

Extrinsic and Intrinsic Pathways of Hemostasis01:20

Extrinsic and Intrinsic Pathways of Hemostasis

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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...
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Anticoagulant Drugs: Low-Molecular-Weight Heparins01:30

Anticoagulant Drugs: Low-Molecular-Weight Heparins

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Hemostasis is a crucial process that prevents excessive blood loss from damaged blood vessels. It involves various mechanisms such as vasoconstriction, platelet adhesion and activation, and fibrin formation. The importance of each mechanism depends on the type of vessel injury. In contrast, thrombosis is the abnormal formation of a blood clot within the blood vessels, leading to potential complications if the clot obstructs blood flow. Thrombosis can be caused by increased coagulability of the...
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Coagulation01:09

Coagulation

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The coagulation phase is a critical part of the body's process to prevent blood loss following injury to blood vessels. It involves chemical reactions that form a clot to seal the injured area. The clotting process begins shortly after injury, within 15-20 seconds for severe damage and 1-2 minutes for minor injuries.
During the coagulation phase, clotting factors, or procoagulants, play a vital role in initiating and progressing the coagulation cascade. This cascade is a series of reactions...
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Coagulation01:06

Coagulation

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Colloidal solids are solid particles suspended in solution. They are usually negatively charged, attracting a compact primary layer of positively charged ions, which attract more counterions to form an electrical double layer. Electrostatic repulsion between the charged double layers prevents the particles from colliding, stabilizing the colloids. These solids are often undesirable because they can contain toxins that are difficult to remove. Coagulation is a technique that helps aggregate and...
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Introduction to Hemostasis01:05

Introduction to Hemostasis

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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,...
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Clot Retraction and Fibrinolysis01:16

Clot Retraction and Fibrinolysis

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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.
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Related Experiment Video

Updated: Dec 26, 2025

Visualization of Neutrophil Extracellular Traps in Mesenteric Venules After Mesenteric Ischemia-Reperfusion Injury via Intravital Microscopy
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Visualization of Neutrophil Extracellular Traps in Mesenteric Venules After Mesenteric Ischemia-Reperfusion Injury via Intravital Microscopy

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TMEM173 Drives Lethal Coagulation in Sepsis.

Hui Zhang1, Ling Zeng2, Min Xie1

  • 1Department of Pediatrics, Xiangya Hospital, Central South University, Changsha, Hunan 410008, China.

Cell Host & Microbe
|March 7, 2020
PubMed
Summary

Myeloid TMEM173 regulates blood clotting during bacterial infections via calcium release and Gasdermin D (GSDMD) activation, independent of interferon. This pathway is crucial for sepsis survival and patient mortality.

Keywords:
ER stressGSDMDSTINGTMEM173calciumcoagulationinflammasomepyroptosissepsistissue factor

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Area of Science:

  • Immunology
  • Hematology
  • Molecular Biology

Background:

  • TMEM173/STING-dependent innate immunity is vital for inflammatory disorders.
  • The role of myeloid TMEM173 in coagulation during bacterial infections remains unclear.

Purpose of the Study:

  • To elucidate the mechanism by which myeloid TMEM173 regulates coagulation in bacterial infections.
  • To investigate the TMEM173-GSDMD-F3 pathway's role in sepsis and its potential as a therapeutic target.

Main Methods:

  • Investigated TMEM173's role in myeloid cells during bacterial infection models.
  • Utilized genetic and pharmacological inhibition of the TMEM173-GSDMD-F3 pathway.
  • Analyzed TMEM173 pathway upregulation in sepsis patients with disseminated intravascular coagulation.

Main Results:

  • Myeloid TMEM173 regulates coagulation independently of type I interferon response.
  • TMEM173 binding to ITPR1 controls calcium release, activating Gasdermin D (GSDMD) and initiating blood coagulation via F3.
  • Inhibition of the TMEM173-GSDMD-F3 pathway improved survival in sepsis models.
  • TMEM173 pathway upregulation correlated with sepsis severity and mortality.

Conclusions:

  • TMEM173 is a critical regulator of blood clotting in lethal bacterial infections.
  • The TMEM173-GSDMD-F3 pathway represents a novel mechanism linking innate immunity and coagulation.
  • Targeting this pathway offers a potential therapeutic strategy for sepsis and associated coagulopathies.