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Related Concept Videos

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...
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...
Cerebral Edema ll: Pathophysiology01:22

Cerebral Edema ll: Pathophysiology

Vasogenic edema is a major form of cerebral edema characterized by abnormal accumulation of fluid in the brain’s extracellular space due to disruption of the blood–brain barrier (BBB). The BBB is a specialized structure composed of endothelial cells connected by tight junctions, supported by astrocytic endfeet and a basement membrane. Under normal conditions, it tightly regulates the movement of ions, proteins, and solutes between the bloodstream and brain parenchyma. When this barrier loses...
Cytotoxic Edema: Pathophysiology01:21

Cytotoxic Edema: Pathophysiology

Cytotoxic edema is a form of cerebral edema characterized by intracellular swelling of neurons, astrocytes, and other glial cells. It develops when the mechanisms responsible for maintaining ionic gradients across the cell membrane become impaired. Under normal physiological conditions, the sodium–potassium ATPase actively transports sodium ions out of the cell and potassium ions into the cell, preserving osmotic balance and enabling electrical signaling. This pump requires a continuous supply...
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...
Cellular Injury IV: Necrosis01:16

Cellular Injury IV: Necrosis

Necrosis is a form of irreversible cell death caused by severe injury such as ischemia, toxins, or trauma. Unlike programmed cell death, it is an uncontrolled, pathological process that typically provokes inflammation in surrounding tissues.Pathophysiologic ChangesNecrosis begins when cells sustain critical damage, leading to swelling of organelles, particularly mitochondria, and rapid ATP depletion. As energy levels decline, membrane ion pumps fail, leading to calcium influx and eventually,...

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Related Experiment Video

Updated: Jun 26, 2026

Stretch in Brain Microvascular Endothelial Cells (cEND) as an In Vitro Traumatic Brain Injury Model of the Blood Brain Barrier
07:19

Stretch in Brain Microvascular Endothelial Cells (cEND) as an In Vitro Traumatic Brain Injury Model of the Blood Brain Barrier

Published on: October 26, 2013

Extracellular Mitochondria Mediate Endothelial Injury After Traumatic Brain Injury.

Lujia Tang1,2,3, Yafan Liu1, Kaifeng Pang1

  • 1Department of Neurosurgery, State Key Laboratory of Experimental Hematology, Tianjin Neurological Institute (L.T., Y. Liu, K.P., Y.Z., X.Z., P.Z., Z. Zhou, H.Z., T.M., J.Z., Z. Zhao), Tianjin Medical University General Hospital, China.

Arteriosclerosis, Thrombosis, and Vascular Biology
|June 25, 2026
PubMed
Summary
This summary is machine-generated.

Extracellular mitochondria (exMt) in blood cause endothelial dysfunction after traumatic brain injury (TBI). These exMt trigger inflammation and cell death, revealing a new mechanism of TBI-induced injury.

Keywords:
brain injuries, traumaticendothelial cellsmitophagyneuroinflammatory diseasesreactive oxygen species

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A Preclinical Controlled Cortical Impact Model for Traumatic Hemorrhage Contusion and Neuroinflammation

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Last Updated: Jun 26, 2026

Stretch in Brain Microvascular Endothelial Cells (cEND) as an In Vitro Traumatic Brain Injury Model of the Blood Brain Barrier
07:19

Stretch in Brain Microvascular Endothelial Cells (cEND) as an In Vitro Traumatic Brain Injury Model of the Blood Brain Barrier

Published on: October 26, 2013

Controlled Cortical Impact Model for Traumatic Brain Injury
05:30

Controlled Cortical Impact Model for Traumatic Brain Injury

Published on: August 5, 2014

A Preclinical Controlled Cortical Impact Model for Traumatic Hemorrhage Contusion and Neuroinflammation
06:50

A Preclinical Controlled Cortical Impact Model for Traumatic Hemorrhage Contusion and Neuroinflammation

Published on: June 10, 2020

Area of Science:

  • Neuroscience
  • Cell Biology
  • Immunology

Background:

  • Traumatic brain injury (TBI) causes widespread endothelial dysfunction, leading to secondary complications like edema and inflammation.
  • The mechanisms driving endothelial dysfunction beyond the initial injury site are not fully understood.
  • Extracellular mitochondria (exMt) were identified as a significant component of brain-derived extracellular vesicles post-TBI.

Purpose of the Study:

  • To investigate the role of extracellular mitochondria (exMt) in TBI-induced endothelial dysfunction.
  • To elucidate the mechanism by which exMt contribute to secondary injury following TBI.

Main Methods:

  • Circulating exMt levels were measured in TBI patients and mice.
  • In vitro and in vivo experiments assessed exMt effects on endothelial cells.
  • Mechanistic studies focused on Cavin-1-dependent endocytosis, mitophagy, lysosomal function, and apoptosis.
  • Studies utilized Cavin-1 knockdown cells and deficient mice for validation.

Main Results:

  • Elevated exMt were detected in the blood of TBI patients.
  • Endothelial cells internalized exMt via Cavin-1-dependent endocytosis.
  • exMt induced vascular leakage and inflammation in vitro.
  • Infusion of exMt into naive mice replicated TBI-associated brain and lung changes.
  • exMt triggered mitophagy but impaired lysosomal function, causing endothelial cell apoptosis.

Conclusions:

  • This study identifies a novel subcellular mechanism for endothelial dysfunction following TBI.
  • Extracellular mitochondria play a critical role in mediating secondary injury after TBI.