Ferroptosis-centered Disease Response Information

General Information of the Disease (ID: DIS00134)
Name
Kidney calculus
ICD
ICD-11: GB70
Full List of Target(s) of This Ferroptosis-centered Disease
Nuclear receptor coactivator 4 (NCOA4)
 Target Info 
In total 1 item(s) under this target
Experiment 1 Reporting the Ferroptosis-centered Disease Response by This Target [1]
Target for Ferroptosis Driver
Responsed Disease Kidney calculus [ICD-11: GB70]
Responsed Drug Oxalate Investigative
 Drug Info 
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Autophagy hsa04140
Cell Process Cell ferroptosis
Cell autophagy
In Vitro Model HK-2 cells Normal Homo sapiens CVCL_0302
In Vivo Model
Five-week-old male SD (Sprague-Dawley) rats (130-180 g) were used as experimental subjects. The control group had a normal diet, and the stone model group drank water containing 0.75% ethylene glycol. After feeding for one month, rats were sacrificed, and their kidneys were removed and subjected to silver nitrate staining, immunohistochemistry, and western blotting on the specimens of the normal control group and the kidney stone model group to explore the expression of NCOA4 in kidney stone model rats.

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Response regulation Oxalate activates autophagy to induce ferroptosis of renal tubular epithelial cells and participates in the formation of kidney stones. Moreover, after oxalate treatment, overexpression of the BENC1 gene increased cell oxidative damage and ferroptosis. In addition, knockdown of NCOA4 reversed the effect of oxalate-induced ferroptosis in HK-2 cells.
Unspecific Target
In total 1 item(s) under this target
Experiment 1 Reporting the Ferroptosis-centered Disease Response by This Target [2]
Responsed Disease Kidney calculus [ICD-11: GB70]
Responsed Regulator Caveolin-1 (CAV1) Suppressor
 Regulator Info 
Pathway Response Ferroptosis hsa04216
Autophagy hsa04140
Wnt signaling pathway hsa04310
Cell Process Cell ferroptosis
Cell autophagy
In Vitro Model HK-2 cells Normal Homo sapiens CVCL_0302
In Vivo Model
Six male SD rats (8 weeks old, 300 g) were purchased from the experimental Animal Centre of Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology. The two groups included control group and the glyoxylic acid group, rats in the glyoxylic acid group were intraperitoneally injected with glyoxylic acid (10.5 mg/ml, 6.66 ml/kg, Macklin, Shanghai, China) every day for 9 days. All rats were given free access to food and maintained in an environment of 25 during the experimental period. 7% chloral hydrate (0.7 ml/100 g) was used for anaesthesia.

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Response regulation Calcium oxalate (CaOx) is the most common type of kidney stone. CAV1 could ameliorate autophagy-dependent ferroptosis through the LRP6/Wnt/-Catenin axis, and finally alleviate CaOx stone formation.
References
Ref 1 Oxalate Activates Autophagy to Induce Ferroptosis of Renal Tubular Epithelial Cells and Participates in the Formation of Kidney Stones. Oxid Med Cell Longev. 2021 Oct 6;2021:6630343. doi: 10.1155/2021/6630343. eCollection 2021.
Ref 2 CAV1 alleviated CaOx stones formation via suppressing autophagy-dependent ferroptosis. PeerJ. 2022 Sep 15;10:e14033. doi: 10.7717/peerj.14033. eCollection 2022.