Portal:AOP/Mission

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Current revision (11:06, 19 December 2017) (view source)
 
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The proposed list of the first set of AOPs to be created (to be defined soon):
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The proposed list of the first set of AOPs to be created, some are more defined than others:
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*
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* Chemical-induced bile duct obstruction leads to liver failure
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*
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* Chemical-induced bile duct obstruction leads to nephrotoxicity
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*
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* Inhibition of N-linked glycosylation leads to liver injury
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*
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* Mitochondrial complex inhibition leading to liver injury
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*
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* Inhibition of mitochondrial complex I of nigra-striatal neurons leads to parkinsonian motor deficits
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* Peripheral neuropathy caused by microtubule interacting drugs
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* Oxidative reactivity leads to chemical-induced fanconi syndrome
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* Binding to complex I of the electron transport chain leading to chemical-induced Fanconi syndrome
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* Intracellular accumulation of chemicals via the megalin/cubulin system leading to tubulonephritis
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* Oxidant-induced pulmonary emphysema
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* α-diketone-induced bronchiolitis obliterans
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* HDAC inhibition leads to neural tube defects
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* Cyp17 inhibition leads to undescended testes
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* Oxidative stress-induced liver injury
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* IKK complex inhibition leads to liver failure
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* HDAC inhibition leads to impaired craniofacial development

Current revision

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, some are more defined than others:

  • Chemical-induced bile duct obstruction leads to liver failure
  • Chemical-induced bile duct obstruction leads to nephrotoxicity
  • Inhibition of N-linked glycosylation leads to liver injury
  • Mitochondrial complex inhibition leading to liver injury
  • Inhibition of mitochondrial complex I of nigra-striatal neurons leads to parkinsonian motor deficits
  • Peripheral neuropathy caused by microtubule interacting drugs
  • Oxidative reactivity leads to chemical-induced fanconi syndrome
  • Binding to complex I of the electron transport chain leading to chemical-induced Fanconi syndrome
  • Intracellular accumulation of chemicals via the megalin/cubulin system leading to tubulonephritis
  • Oxidant-induced pulmonary emphysema
  • α-diketone-induced bronchiolitis obliterans
  • HDAC inhibition leads to neural tube defects
  • Cyp17 inhibition leads to undescended testes
  • Oxidative stress-induced liver injury
  • IKK complex inhibition leads to liver failure
  • HDAC inhibition leads to impaired craniofacial development


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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