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, some are more defined than others: |
| - | * | + | * Decrease of lysosomal phospholipase activity leads to phospholipidosis |
| - | * | + | * Immune-mediated liver injury |
| - | * | + | * Reduced mitochondrial activity leads to cholestasis |
| - | * | + | * Liver fibrosis |
| - | * | + | * Unfolded protein response-mediated liver toxicity |
| + | * Increased ROS levels lead to hepatotoxicity | ||
| + | * Inhibition of mitochondrial complex I of nigra-striatal neurons leads to parkinsonian motor deficits | ||
| + | * Decreased ATP production leads to neurodegeneration | ||
| + | * 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... | ||
| + | * Oxidative stress leads to COPD | ||
| + | * Activation of Smad signaling leads to pulmonary fibrosis | ||
| + | * Impaired HDAC leads to limbosacral spina bifida | ||
| + | * HDAC inhibition leads to neural tube defects | ||
| + | * Cyt p450 inhibition leads to Feminization and Masculinization | ||
| + | * Estrogen/androgen ... | ||
| + | * Bone malformation | ||
| + | * Oxidative stress-induced hepatoxicity | ||
| + | * Inflammatory cytokine-induced cell death | ||
| + | * HDAC inhibition leads to impaired craniofacial development | ||
Revision as of 10:51, 14 August 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:
- Decrease of lysosomal phospholipase activity leads to phospholipidosis
- Immune-mediated liver injury
- Reduced mitochondrial activity leads to cholestasis
- Liver fibrosis
- Unfolded protein response-mediated liver toxicity
- Increased ROS levels lead to hepatotoxicity
- Inhibition of mitochondrial complex I of nigra-striatal neurons leads to parkinsonian motor deficits
- Decreased ATP production leads to neurodegeneration
- 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...
- Oxidative stress leads to COPD
- Activation of Smad signaling leads to pulmonary fibrosis
- Impaired HDAC leads to limbosacral spina bifida
- HDAC inhibition leads to neural tube defects
- Cyt p450 inhibition leads to Feminization and Masculinization
- Estrogen/androgen ...
- Bone malformation
- 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
