General Information of the Disease (ID: DIS00141)
Name
Immunoglobulin A nephropathy
ICD
ICD-11: MF8Y
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.
References
Ref 1 Downregulation of PPAR mediates FABP1 expression, contributing to IgA nephropathy by stimulating ferroptosis in human mesangial cells. Int J Biol Sci. 2022 Aug 29;18(14):5438-5458. doi: 10.7150/ijbs.74675. eCollection 2022.