Portal:AOP/Mission

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The proposed list of the first set of AOPs to be created:
The proposed list of the first set of AOPs to be created:
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* Inhibition of β-oxidation leads to liver steatosis
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*Inhibition of β-oxidation leads to liver steatosis
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* HDAC inhibition, folate antagonism and oxidative stress lead to teratogenicity
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*HDAC inhibition leads to teratogenicity
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* Oxidative stress leads to hepatotoxicity
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*ROS formation leads to teratogenicity
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* Oxidative stress leads to nephrotoxicity
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*Oxidative stress leads to hepatotoxicity
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* Disturbance of the respiratory chain leads to mitotoxicity
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*Oxidative stress leads to nephrotoxicity
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* PPAR activation leads to hepatoxicity
+
*Disturbance of the respiratory chain leads to mitotoxicity
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* OAT overactivation leads to nephrotoxicity
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*PPAR activation leads to hepatoxicity
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* PXR activation leads to liver steatosis
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*OAT overactivation leads to nephrotoxicity
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* NAPQI production causes hepatotoxicity
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*PXR activation leads to liver steatosis
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* MTP impairment leads to hepatotoxicity
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*NAPQI production causes hepatotoxicity
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* CYP51 inhibition causes embryotoxicity
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*MTP impairment leads to hepatotoxicity
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* Epithelial damage leads to popcorn lung
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*CYP51 inhibition causes embryotoxicity
 +
*Epithelial damage leads to popcorn lung
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Revision as of 13:20, 6 April 2017

The purpose of this portal is to create a collection of AOPs on the molecular level for the AOPs that are, or will be created for the EU-ToxRisk program, in which Open PHACTS Foundation (OPF) is responsible for AOP creation. The subjects of the first AOPs are linked to the use cases of the EU-ToxRisk program, and there will be a team of experts involved in the creation of each AOP.


The proposed list of the first set of AOPs to be created:

  • Inhibition of β-oxidation leads to liver steatosis
  • HDAC inhibition leads to teratogenicity
  • ROS formation leads to teratogenicity
  • Oxidative stress leads to hepatotoxicity
  • Oxidative stress leads to nephrotoxicity
  • Disturbance of the respiratory chain leads to mitotoxicity
  • PPAR activation leads to hepatoxicity
  • OAT overactivation leads to nephrotoxicity
  • PXR activation leads to liver steatosis
  • NAPQI production causes hepatotoxicity
  • MTP impairment leads to hepatotoxicity
  • CYP51 inhibition causes embryotoxicity
  • Epithelial damage leads to popcorn lung


Basic strategies and principles for general AOPs are described in this paper:

Villeneuve et al. (2014). Adverse Outcome Pathway (AOP) Development I: Strategies and Principles. Toxicological Sciences PubMed

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