Portal:AOP/Mission
From WikiPathways
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The proposed list of the first set of AOPs to be created, some are more defined than others: | The proposed list of the first set of AOPs to be created, some are more defined than others: | ||
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* Reduced mitochondrial activity leads to cholestasis | * Reduced mitochondrial activity leads to cholestasis | ||
* Liver fibrosis | * Liver fibrosis | ||
* Unfolded protein response-mediated liver toxicity | * Unfolded protein response-mediated liver toxicity | ||
| - | * | + | * Mitotoxicity-mediated hepatotoxicity |
* Inhibition of mitochondrial complex I of nigra-striatal neurons leads to parkinsonian motor deficits | * Inhibition of mitochondrial complex I of nigra-striatal neurons leads to parkinsonian motor deficits | ||
| - | |||
* Peripheral neuropathy caused by microtubule interacting drugs | * Peripheral neuropathy caused by microtubule interacting drugs | ||
* Oxidative reactivity leads to chemical-induced fanconi syndrome | * Oxidative reactivity leads to chemical-induced fanconi syndrome | ||
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* Compound accumulation via Megalin/Cubilin uptake leads to acute and chronic kidney disease | * Compound accumulation via Megalin/Cubilin uptake leads to acute and chronic kidney disease | ||
* Renal proximal tubular uptake via organic cation transporters leads to... | * Renal proximal tubular uptake via organic cation transporters leads to... | ||
| - | * | + | * Oxidant-induced pulmonary emphysema |
| - | + | * α-diketone-induced bronchiolitis obliterans | |
| - | * | + | |
* HDAC inhibition leads to neural tube defects | * HDAC inhibition leads to neural tube defects | ||
* Cyt p450 inhibition leads to Feminization and Masculinization | * Cyt p450 inhibition leads to Feminization and Masculinization | ||
* Estrogen/androgen ... | * Estrogen/androgen ... | ||
| - | |||
* Oxidative stress-induced hepatoxicity | * Oxidative stress-induced hepatoxicity | ||
* Inflammatory cytokine-induced cell death | * Inflammatory cytokine-induced cell death | ||
Revision as of 14:47, 18 October 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, some are more defined than others:
- Reduced mitochondrial activity leads to cholestasis
- Liver fibrosis
- Unfolded protein response-mediated liver toxicity
- Mitotoxicity-mediated hepatotoxicity
- 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
- Oxidative reactivity leads to acceleration of chronic kidney disease
- Compound accumulation via Megalin/Cubilin uptake leads to acute and chronic kidney disease
- Renal proximal tubular uptake via organic cation transporters leads to...
- Oxidant-induced pulmonary emphysema
- α-diketone-induced bronchiolitis obliterans
- HDAC inhibition leads to neural tube defects
- Cyt p450 inhibition leads to Feminization and Masculinization
- Estrogen/androgen ...
- Oxidative stress-induced hepatoxicity
- Inflammatory cytokine-induced cell death
- 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
