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Related Concept Videos

Spinal Cord Injury ll: Pathophysiology01:14

Spinal Cord Injury ll: Pathophysiology

Spinal cord injury progresses through two interconnected phases: primary injury and secondary injury.Primary InjuryPrimary injury happens at the moment of trauma and involves immediate mechanical damage to the spinal cord.Compression happens when broken vertebrae, herniated discs, or accumulating blood (such as a hematoma) press directly against the spinal cord, distorting its normal shape and function. In cases of contusion, the cord is bruised by a blunt force (like penetrating injuries or...
Cellular Injury II: Classification01:21

Cellular Injury II: Classification

Cellular injury is any process that disrupts a cell’s ability to maintain homeostasis, leading to structural or functional changes. It is broadly classified based on etiology (cause) and mechanism of damage.Classification by EtiologyCellular injury may result from several causes. Hypoxic injury happens due to reduced oxygen delivery, most commonly from inadequate blood supply, such as arterial obstruction; for example, coronary artery thrombosis can cause myocardial infarction. Chemical injury...
Hemorrhagic Stroke ll: Pathophysiology01:29

Hemorrhagic Stroke ll: Pathophysiology

A hemorrhagic stroke develops when a cerebral blood vessel ruptures, allowing blood to escape into the surrounding brain tissue, as in intracerebral hemorrhage (ICH), or into the subarachnoid space, as in subarachnoid hemorrhage (SAH). Because the skull is a rigid compartment, the sudden presence of extravascular blood rapidly increases intracranial pressure and compresses adjacent neural structures, leading to immediate tissue injury and impaired cerebral perfusion.Mass Effect and Primary...
Secondary Spinal Cord Injury llI: Pathophysiology01:25

Secondary Spinal Cord Injury llI: Pathophysiology

Early Ischemia and Ionic ImbalanceWithin minutes of spinal cord injury, a secondary cascade begins, progressing over hours to weeks. Vascular damage reduces blood flow, causing ischemia and mitochondrial dysfunction. ATP depletion leads to ion pump failure, membrane depolarization, sodium influx, potassium efflux, and water accumulation, resulting in cellular swelling. Increased intracellular calcium further disrupts mitochondria and accelerates cellular injury.Excitotoxicity and Neuronal...
Venous Thrombosis I: Introduction01:30

Venous Thrombosis I: Introduction

Venous thrombosis, the most common disorder of the veins, involves the formation of a thrombus or blood clot associated with vein inflammation. It can be classified as either superficial vein thrombosis or deep vein thrombosis.Superficial Vein Thrombosis: This involves the formation of a thrombus in a superficial vein, usually the greater or lesser saphenous vein. Though less severe than deep vein thrombosis (DVT), SVT can lead to complications if untreated.Deep Vein Thrombosis (DVT): This...
Traumatic Brain Injury l: Introduction01:28

Traumatic Brain Injury l: Introduction

DefinitionTraumatic brain injury, or TBI, is a disturbance of normal brain function induced by an external mechanical force, such as a direct blow to the head or a penetrating injury. It can affect both brain structure and function, producing a wide range of clinical outcomes. TBI is a heterogeneous condition, meaning its effects may differ based on the type, location, and severity of the injury.Basis of ClassificationTBI is classified based on severity, injury mechanism, or pathophysiology. In...

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Updated: Jul 15, 2026

An In Vivo Duo-color Method for Imaging Vascular Dynamics Following Contusive Spinal Cord Injury
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Published on: December 31, 2017

Trail and vascular injury.

Jose L Martin-Ventura1, Begona Munoz-Garcia, Jesus Egido

  • 1Vascular Research Lab, Fundacion Jimenez Diaz, Autonoma University, Madrid, Spain. jlmartin@fjd.es

Frontiers in Bioscience : a Journal and Virtual Library
|May 9, 2007
PubMed
Summary

Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) may promote vascular inflammation and cell death in atherosclerosis. Plasma levels of TRAIL and osteoprotegerin (OPG) are being investigated as potential markers for vascular injury.

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Area of Science:

  • Cardiovascular biology
  • Immunology
  • Molecular medicine

Background:

  • Cardiovascular diseases are a leading cause of death, driven by atherosclerosis, characterized by arterial wall thickening and atheromatous plaque formation.
  • Key atherogenesis mechanisms include lipoprotein retention, endothelial activation, smooth muscle cell proliferation, macrophage infiltration, and apoptosis.
  • Members of the tumor necrosis factor (TNF) family, including TNF-related apoptosis-inducing ligand (TRAIL) and its receptors (TRAIL-Rs, OPG), are found in atherosclerotic plaques.

Purpose of the Study:

  • To review the role of TRAIL and its receptors in the mechanisms of atherothrombosis.
  • To discuss the controversial effects of TRAIL on vascular cell inflammation and apoptosis.
  • To explore the potential of plasma TRAIL and OPG levels as biomarkers for vascular injury.

Main Methods:

  • Literature review of studies on TRAIL and its receptors in atherogenesis.
  • Analysis of in vivo studies investigating TRAIL's role in vascular injury.
  • Examination of research on soluble TNF-superfamily members in human plasma.

Main Results:

  • TRAIL and its receptors are present in human atherosclerotic plaques.
  • Data on TRAIL's effects on vascular cell inflammation and apoptosis remain controversial.
  • Recent in vivo studies suggest TRAIL may have pro-inflammatory and pro-apoptotic effects in vascular injury.

Conclusions:

  • TRAIL and its receptors are implicated in atherothrombosis.
  • Further research is needed to clarify TRAIL's precise role in vascular inflammation and apoptosis.
  • Plasma levels of TRAIL and OPG may serve as potential biomarkers for vascular injury.