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Related Concept Videos

Urea Cycle01:23

Urea Cycle

The urea cycle describes how liver cells convert ammonia to urea. Ammonia is a toxic waste product of protein catabolism. Land animals must convert ammonia into the less toxic urea which can be safely eliminated by the kidneys through urine. Marine animals excrete ammonia directly, and the surrounding water dilutes the ammonia to safe levels.
Hepatic Encephalopathy01:29

Hepatic Encephalopathy

DefinitionHepatic encephalopathy is a reversible neurologic syndrome that results from advanced liver dysfunction or portosystemic shunting. It leads to disturbances in cognition, behavior, and motor function due to the brain’s exposure to gut-derived toxins that the liver fails to detoxify.EtiologyThis condition develops either in the setting of acute fulminant hepatitis or progressively during chronic liver disease, such as cirrhosis and portal hypertension. Portosystemic shunting—including...
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  3. Lox-1 Rewires Glutamine Ammonia Metabolism To Drive Liver Fibrosis.
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  3. Lox-1 Rewires Glutamine Ammonia Metabolism To Drive Liver Fibrosis.

Related Experiment Video

Glutamine Flux Imaging Using Genetically Encoded Sensors
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LOX-1 rewires glutamine ammonia metabolism to drive liver fibrosis.

Ruihua Huang1, Hanyu Cui1, Mohammed Abdulaziz Yahya Ali Alshami1

  • 1Xiangya School of Pharmaceutical Sciences, Central South University, Changsha 410013, China.

Molecular Metabolism
|April 3, 2025

View abstract on PubMed

Summary
This summary is machine-generated.

Lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) promotes liver fibrosis by activating hepatic stellate cells and altering ammonia metabolism. Targeting LOX-1 offers a promising therapeutic strategy for liver fibrosis.

Keywords:
GLSLOX-1Liver fibrosisUrea cycle

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Area of Science:

  • Hepatology
  • Molecular Biology
  • Metabolic Disease

Background:

  • Liver fibrosis is a critical factor in chronic liver disease prognosis.
  • Lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) shows potential in fibrotic disease research.
  • The precise role and mechanisms of LOX-1 in liver fibrosis progression are not fully understood.

Purpose of the Study:

  • To investigate the role of LOX-1 in liver fibrosis progression.
  • To elucidate the underlying molecular mechanisms by which LOX-1 influences liver fibrosis.
  • To explore LOX-1 as a potential therapeutic target for liver fibrosis.

Main Methods:

  • LOX-1 expression analysis in human and rodent liver fibrosis tissues.
  • Induction of liver fibrosis in LOX-1 knockout rats using CCl4 or MCD diet.
  • Transcriptomic and metabolomic analyses to identify LOX-1's mechanism of action.

    • Main Results:

    • LOX-1 exacerbates liver fibrosis by promoting hepatic stellate cell activation.
    • Deletion of LOX-1 reversed liver fibrosis development.
    • LOX-1 reprograms glutamine metabolism via glutaminase (GLS) isoform switching, impacting ammonia metabolism and the urea cycle.

    Conclusions:

    • LOX-1 plays a pivotal role in liver fibrosis progression.
    • LOX-1 regulates hepatic ammonia metabolism, offering new pathological insights.
    • Targeting LOX-1 presents a promising therapeutic strategy for antifibrotic therapy.