API

Event: 459

Key Event Title

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Increased, Liver Steatosis

Short name

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Increased, Liver Steatosis

Biological Context

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Level of Biological Organization
Organ


Organ term

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Organ term
liver


Key Event Components

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Process Object Action

Key Event Overview


AOPs Including This Key Event

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Stressors

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Taxonomic Applicability

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Term Scientific Term Evidence Link
Vertebrates Vertebrates High NCBI

Life Stages

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Life stage Evidence
All life stages High

Sex Applicability

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Term Evidence
Unspecific High

Key Event Description

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Biological state: liver steatosis is the inappropriate storage of fat in hepatocytes.

Biological compartment: steatosis is generally an organ-level diagnosis; however, the pathology occurs within the hepatocytes.

Role in biology: steatosis is an adverse endpoint. 

 

Description from EU-ToxRisk:

Activation of stellate cells results in collagen accumulation and change in extracellular matrix composition in the liver causing fibrosis. (Landesmann, 2016)(Koo et al 2016)


How It Is Measured or Detected

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Steatosis is measured by lipidomics approaches that measure lipid levels, or by histology.


Domain of Applicability

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Steatosis is the result of perturbations in well-known metabolic pathways that are well-studied and well-known in many taxa.


Regulatory Significance of the Adverse Outcome

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Steatosis is a regulatory endpoint and has been used as an endpoint in many US EPA assessments, including IRIS assessments.


References

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Landesmann, B. (2016). Adverse Outcome Pathway on Protein Alkylation Leading to Liver Fibrosis, (2).

https://doi.org/10.1016/j.molcel.2005.08.010

Koo, J. H., Lee, H. J., Kim, W., & Kim, S. G. (2016). Endoplasmic Reticulum Stress in Hepatic Stellate Cells Promotes Liver Fibrosis via PERK-Mediated Degradation of HNRNPA1 and Up-regulation of SMAD2. Gastroenterology, 150(1), 181–193.e8. https://doi.org/10.1053/j.gastro.2015.09.039