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Liver Regeneration01:24

Liver Regeneration

The liver is an important organ in vertebrates that plays an essential role in metabolism. It is also responsible for storing and redistributing nutrients such as carbohydrates, fats, and vitamins in the body. Additionally, the liver releases bile salts which are critical for digesting food and eliminating toxic metabolites from the body.
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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...
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Related Experiment Video

Updated: Jun 29, 2026

Rat Model of Widespread Cerebral Cortical Demyelination Induced by an Intracerebral Injection of Pro-Inflammatory Cytokines
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Circulating Cathepsin D Exacerbates Injury-Induced Brain Damage by Promoting Neutrophil Infiltration Into the Brain.

Yu Liang1, Dan Zhao1,2, Peng-Fei Wu2

  • 1Department of Developmental Cell Biology, Key Laboratory of Cell Biology, Ministry of Public Health, and Key Laboratory of Medical Cell Biology, Ministry of Education China Medical University Shenyang China.

Journal of the American Heart Association
|October 28, 2025
PubMed
Summary

High levels of circulating Cathepsin D (CTSD) worsen brain injury by activating endothelium and increasing neutrophil infiltration. Reducing CTSD levels protects against brain damage and improves motor function recovery.

Keywords:
VCAM‐1brain endothelial cellsbrain injurycathepsin Dneutrophil infiltration

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Area of Science:

  • Neuroscience
  • Immunology
  • Molecular Biology

Background:

  • Vascular endothelium and leukocyte communication regulates brain inflammation.
  • Elevated plasma Cathepsin D (CTSD) is linked to vascular events.
  • The effect of circulating CTSD on endothelial function is unknown.

Purpose of the Study:

  • To investigate the role of circulating CTSD in brain injury.
  • To determine if CTSD affects endothelial activation and leukocyte infiltration.
  • To assess the therapeutic potential of reducing CTSD levels.

Main Methods:

  • Used transgenic mice with high (hCTSDhi) or low (CTSDMono knockout) circulating CTSD levels.
  • Subjected mice to traumatic and ischemic brain injury.
  • Performed single-cell RNA sequencing to analyze brain gene expression.
  • Investigated the mechanism of CTSD-induced endothelial activation via VCAM-1.

Main Results:

  • hCTSDhi mice exhibited increased neutrophil infiltration and worsened motor deficits after brain injury.
  • Circulating CTSD functions as nonenzymatic pro-CTSD, activating brain endothelium.
  • Pro-CTSD upregulates VCAM-1 expression, facilitating neutrophil transmigration.
  • Genetic reduction of CTSD attenuated injury-induced neutrophil infiltration and motor deficits.

Conclusions:

  • Circulating prototype CTSD exacerbates brain damage following injury.
  • CTSD promotes neutrophil infiltration by upregulating endothelial VCAM-1.
  • Reducing CTSD levels offers a potential therapeutic strategy for brain injury.