Ferroptosis-centered Disease Response Information
General Information of the Disease (ID: DIS00001)
Name |
HIV Infection
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ICD |
ICD-11: 1C60
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Full List of Target(s) of This Ferroptosis-centered Disease
Unspecific Target
In total 1 item(s) under this target | ||||
Experiment 1 Reporting the Ferroptosis-centered Disease Response by This Target | [1] | |||
Responsed Disease | HIV-associated neurocognitive disorder [ICD-11: 1C60-1C62] | |||
Responsed Drug | Methamphetamine | Investigative | ||
Responsed Regulator | Cellular tumor antigen p53 (TP53) | Driver | ||
Pathway Response | Ferroptosis | hsa04216 | ||
Fatty acid metabolism | hsa01212 | |||
Cell Process | Cell ferroptosis | |||
In Vitro Model | BV-2 cells | Normal | Mus musculus | CVCL_0182 |
Response regulation | Methamphetamine (METH) and HIV-1 lead to oxidative stress and their combined effect increases the risk of HIV-associated neurocognitive disorder (HAND), which may be related to the synergistic ferroptotic impairment in microglia. We found that METH and HIV-1 Tat reduced the expression of ferroptotic protein GPX4 and the cell viability and enhanced the expression of P53 and the level of ferrous iron, while the above indices were significantly improved with pretreatment of ferrostatin-1. | |||
Phospholipid hydroperoxide glutathione peroxidase (GPX4)
In total 1 item(s) under this target | ||||
Experiment 1 Reporting the Ferroptosis-centered Disease Response by This Target | [1] | |||
Target for Ferroptosis | Suppressor | |||
Responsed Disease | HIV-associated neurocognitive disorder [ICD-11: 1C60-1C62] | |||
Responsed Drug | Methamphetamine | Investigative | ||
Pathway Response | Ferroptosis | hsa04216 | ||
Fatty acid metabolism | hsa01212 | |||
Cell Process | Cell ferroptosis | |||
In Vitro Model | BV-2 cells | Normal | Mus musculus | CVCL_0182 |
Response regulation | Methamphetamine (METH) and HIV-1 lead to oxidative stress and their combined effect increases the risk of HIV-associated neurocognitive disorder (HAND), which may be related to the synergistic ferroptotic impairment in microglia. We found that METH and HIV-1 Tat reduced the expression of ferroptotic protein GPX4 and the cell viability and enhanced the expression of P53 and the level of ferrous iron, while the above indices were significantly improved with pretreatment of ferrostatin-1. | |||