Ferroptosis-centered Disease Response Information
General Information of the Disease (ID: DIS00141)
Name |
Immunoglobulin A nephropathy
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ICD |
ICD-11: MF8Y
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Full List of Target(s) of This Ferroptosis-centered Disease
Phospholipid hydroperoxide glutathione peroxidase (GPX4)
In total 2 item(s) under this target | ||||
Experiment 1 Reporting the Ferroptosis-centered Disease Response by This Target | [1] | |||
Target for Ferroptosis | Suppressor | |||
Responsed Disease | Immunoglobulin A nephropathy [ICD-11: MF8Y] | |||
Responsed Regulator | Peroxisome proliferator-activated receptor alpha (PPARA) | Suppressor | ||
Pathway Response | Fatty acid metabolism | hsa01212 | ||
Ferroptosis | hsa04216 | |||
Cell Process | Cell ferroptosis | |||
In Vitro Model | hMCs (Human mesangial cells) | |||
Response regulation | In PPAR lentivirus-transfected HMCs stimulated by Gd-IgA1, ROS, MDA, and ACSL4 were decreased; glutathione and GPX4, and immunofluorescence colocalization of PPAR and GPX4, increased; and damaged mitochondria reduced. Hence, PPAR pathway downregulation can reduce FABP1 expression, affecting GPX4 and ACSL4 levels, causing HMC ferroptosis, and contributing to immunoglobulin A nephropathy (IgAN) pathogenesis. | |||
Experiment 2 Reporting the Ferroptosis-centered Disease Response by This Target | [1] | |||
Target for Ferroptosis | Suppressor | |||
Responsed Disease | Immunoglobulin A nephropathy [ICD-11: MF8Y] | |||
Responsed Regulator | Fatty acid-binding protein, liver (FABP1) | Suppressor | ||
Pathway Response | Fatty acid metabolism | hsa01212 | ||
Ferroptosis | hsa04216 | |||
Cell Process | Cell ferroptosis | |||
In Vitro Model | hMCs (Human mesangial cells) | |||
Response regulation | In PPAR lentivirus-transfected HMCs stimulated by Gd-IgA1, ROS, MDA, and ACSL4 were decreased; glutathione and GPX4, and immunofluorescence colocalization of PPAR and GPX4, increased; and damaged mitochondria reduced. Hence, PPAR pathway downregulation can reduce FABP1 expression, affecting GPX4 and ACSL4 levels, causing HMC ferroptosis, and contributing to immunoglobulin A nephropathy (IgAN) pathogenesis. | |||
Long-chain-fatty-acid--CoA ligase 4 (ACSL4)
In total 2 item(s) under this target | ||||
Experiment 1 Reporting the Ferroptosis-centered Disease Response by This Target | [1] | |||
Target for Ferroptosis | Driver | |||
Responsed Disease | Immunoglobulin A nephropathy [ICD-11: MF8Y] | |||
Responsed Regulator | Peroxisome proliferator-activated receptor alpha (PPARA) | Suppressor | ||
Pathway Response | Fatty acid metabolism | hsa01212 | ||
Ferroptosis | hsa04216 | |||
Cell Process | Cell ferroptosis | |||
In Vitro Model | hMCs (Human mesangial cells) | |||
Response regulation | In PPAR lentivirus-transfected HMCs stimulated by Gd-IgA1, ROS, MDA, and ACSL4 were decreased; glutathione and GPX4, and immunofluorescence colocalization of PPAR and GPX4, increased; and damaged mitochondria reduced. Hence, PPAR pathway downregulation can reduce FABP1 expression, affecting GPX4 and ACSL4 levels, causing HMC ferroptosis, and contributing to immunoglobulin A nephropathy (IgAN) pathogenesis. | |||
Experiment 2 Reporting the Ferroptosis-centered Disease Response by This Target | [1] | |||
Target for Ferroptosis | Driver | |||
Responsed Disease | Immunoglobulin A nephropathy [ICD-11: MF8Y] | |||
Responsed Regulator | Fatty acid-binding protein, liver (FABP1) | Suppressor | ||
Pathway Response | Fatty acid metabolism | hsa01212 | ||
Ferroptosis | hsa04216 | |||
Cell Process | Cell ferroptosis | |||
In Vitro Model | hMCs (Human mesangial cells) | |||
Response regulation | In PPAR lentivirus-transfected HMCs stimulated by Gd-IgA1, ROS, MDA, and ACSL4 were decreased; glutathione and GPX4, and immunofluorescence colocalization of PPAR and GPX4, increased; and damaged mitochondria reduced. Hence, PPAR pathway downregulation can reduce FABP1 expression, affecting GPX4 and ACSL4 levels, causing HMC ferroptosis, and contributing to immunoglobulin A nephropathy (IgAN) pathogenesis. | |||