Ferroptosis Regulator Information
General Information of the Ferroptosis Regulator (ID: REG10404)
Full List of the Ferroptosis Target of This Regulator and Corresponding Disease/Drug Response(s)
SMAD3
can regulate the following target(s), and cause disease/drug response(s). You can browse detail information of target(s) or disease/drug response(s).
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NADPH oxidase 4 (NOX4) [Driver]
In total 1 item(s) under this target | |||||
Experiment 1 Reporting the Ferroptosis Target of This Regulator | [1] | ||||
Target for Ferroptosis | Driver | ||||
Responsed Disease | Unilateral ureteral obstruction | ICD-11: MG30 | |||
Responsed Drug | Tectorigenin | Investigative | |||
Pathway Response | Fatty acid metabolism | hsa01212 | |||
Cell Process | Cell ferroptosis | ||||
In Vitro Model |
mRTECs (Mouse renal tubular epithelial cells) | ||||
In Vivo Model |
The male C57BL/6 mice (8 weeks old, 22-25 g body weight) used in this study were purchased from Dashuo Bio-Technique Co. Ltd. (Chengdu, China) and were maintained in 12 hr of light/12 hr of darkness. The mice were randomly divided into the following 4 groups (n = 8 per group): Sham, UUO, UUO with tectorigenin (20 mg/kg/day, dissolved in saline with 10% dimethyl sulfoxide [DMSO]) or irbesartan (IRB, a positive control, 20 mg/kg/day) treatment. After anesthesia with 1% pentobarbital, the left ureter was exposed through the lower left incision on the midline of the back and blocked by two-point ligation with 40 silk thread as previously described. The Sham-operated mice underwent the same operation but absence of ligation. The tectorigenin and IRB group were administered intraperitoneally with drug daily for 7 consecutive days since surgery. Sham-operated mice and UUO mice were received the equal volume of solvent.
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Response regulation | Tectorigenin exerts as a Smad3 inhibitor to suppress Smad3 activation through an Nox4-dependent mechanism. Tectorigenin protects against unilateral ureteral obstruction by inhibiting Smad3-mediated ferroptosis and fibrosis. | ||||
Cystine/glutamate transporter (SLC7A11) [Driver; Suppressor]
In total 1 item(s) under this target | |||||
Experiment 1 Reporting the Ferroptosis Target of This Regulator | [2] | ||||
Target for Ferroptosis | Suppressor | ||||
Responsed Disease | Chronic kidney disease | ICD-11: GB61 | |||
Responsed Drug | Formononetin | Investigative | |||
Pathway Response | Ferroptosis | hsa04216 | |||
Fatty acid metabolism | hsa01212 | ||||
Cell Process | Cell ferroptosis | ||||
In Vitro Model |
mPRTECs (Mouse primary renal tubular epithelial cells) | ||||
In Vivo Model |
For UUO-induced CKD, the mice were randomly assigned into four groups (n = 6 per group): UUO, UUO + FN, UUO + VST, and Sham. The mice were anesthetized by intraperitoneal injection of pentobarbital sodium(30 mg/kg). Then, UUO surgery orsham operation was performed as previously described. Mice in the UUO + FN group were orally administrated with 40 mg/kg/day FN (dissolved in 10% DMSO). For positive control, mice in UUO + VST group were orally treated with 20 mg/kg/day VST (dissolved in 10% DMSO). Mice in the UUO and Sham groups were given equivalent solvent by oral. All mice were sacrificed 7 days post-UUO. For UUO-induced CKD, the mice were randomly assigned into four groups (n = 6 per group): UUO, UUO + FN, UUO + VST, and Sham. The mice were anesthetized by intraperitoneal injection of pentobarbital sodium (30 mg/kg). Then, UUO surgery or sham operation was performed as previously described. Mice in the UUO + FN group were orally administrated with 40 mg/kg/day FN (dissolved in 10 % DMSO). For positive control, mice in UUO + VST group were orally treated with 20 mg/kg/day VST (dissolved in 10 % DMSO). Mice in the UUO and Sham groups were given equivalent solvent by oral. All mice were sacrificed 7 days post-UUO.
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Response regulation | Formononetin (FN) alleviates chronic kidney disease (CKD) by impeding ferroptosis-associated fibrosis by suppressing the Smad3/ATF3/SLC7A11 signaling and could serve as a candidate therapeutic drug for CKD. In addition, FN also promoted the separation of the Nrf2/Keap1 complex and enhanced Nrf2 nuclear accumulation. | ||||
Chronic kidney disease [ICD-11: GB61]
In total 1 item(s) under this disease | |||||
Experiment 1 Reporting the Ferroptosis-centered Disease Response | [2] | ||||
Target Regulator | Mothers against decapentaplegic homolog 3 (SMAD3) | Protein coding | |||
Responsed Drug | Formononetin | Investigative | |||
Pathway Response | Ferroptosis | hsa04216 | |||
Fatty acid metabolism | hsa01212 | ||||
Cell Process | Cell ferroptosis | ||||
In Vitro Model |
mPRTECs (Mouse primary renal tubular epithelial cells) | ||||
In Vivo Model |
For UUO-induced CKD, the mice were randomly assigned into four groups (n = 6 per group): UUO, UUO + FN, UUO + VST, and Sham. The mice were anesthetized by intraperitoneal injection of pentobarbital sodium(30 mg/kg). Then, UUO surgery orsham operation was performed as previously described. Mice in the UUO + FN group were orally administrated with 40 mg/kg/day FN (dissolved in 10% DMSO). For positive control, mice in UUO + VST group were orally treated with 20 mg/kg/day VST (dissolved in 10% DMSO). Mice in the UUO and Sham groups were given equivalent solvent by oral. All mice were sacrificed 7 days post-UUO. For UUO-induced CKD, the mice were randomly assigned into four groups (n = 6 per group): UUO, UUO + FN, UUO + VST, and Sham. The mice were anesthetized by intraperitoneal injection of pentobarbital sodium (30 mg/kg). Then, UUO surgery or sham operation was performed as previously described. Mice in the UUO + FN group were orally administrated with 40 mg/kg/day FN (dissolved in 10 % DMSO). For positive control, mice in UUO + VST group were orally treated with 20 mg/kg/day VST (dissolved in 10 % DMSO). Mice in the UUO and Sham groups were given equivalent solvent by oral. All mice were sacrificed 7 days post-UUO.
Click to Show/Hide
|
||||
Response regulation | Formononetin (FN) alleviates chronic kidney disease (CKD) by impeding ferroptosis-associated fibrosis by suppressing the Smad3/ATF3/SLC7A11 signaling and could serve as a candidate therapeutic drug for CKD. In addition, FN also promoted the separation of the Nrf2/Keap1 complex and enhanced Nrf2 nuclear accumulation. | ||||
Unilateral ureteral obstruction [ICD-11: MG30]
In total 1 item(s) under this disease | |||||
Experiment 1 Reporting the Ferroptosis-centered Disease Response | [1] | ||||
Target Regulator | Mothers against decapentaplegic homolog 3 (SMAD3) | Protein coding | |||
Responsed Drug | Tectorigenin | Investigative | |||
Pathway Response | Fatty acid metabolism | hsa01212 | |||
Cell Process | Cell ferroptosis | ||||
In Vitro Model |
mRTECs (Mouse renal tubular epithelial cells) | ||||
In Vivo Model |
The male C57BL/6 mice (8 weeks old, 22-25 g body weight) used in this study were purchased from Dashuo Bio-Technique Co. Ltd. (Chengdu, China) and were maintained in 12 hr of light/12 hr of darkness. The mice were randomly divided into the following 4 groups (n = 8 per group): Sham, UUO, UUO with tectorigenin (20 mg/kg/day, dissolved in saline with 10% dimethyl sulfoxide [DMSO]) or irbesartan (IRB, a positive control, 20 mg/kg/day) treatment. After anesthesia with 1% pentobarbital, the left ureter was exposed through the lower left incision on the midline of the back and blocked by two-point ligation with 40 silk thread as previously described. The Sham-operated mice underwent the same operation but absence of ligation. The tectorigenin and IRB group were administered intraperitoneally with drug daily for 7 consecutive days since surgery. Sham-operated mice and UUO mice were received the equal volume of solvent.
Click to Show/Hide
|
||||
Response regulation | Tectorigenin exerts as a Smad3 inhibitor to suppress Smad3 activation through an Nox4-dependent mechanism. Tectorigenin protects against unilateral ureteral obstruction by inhibiting Smad3-mediated ferroptosis and fibrosis. | ||||
Formononetin
[Investigative]
In total 1 item(s) under this drug | |||||
Experiment 1 Reporting the Ferroptosis-centered Drug Response | [2] | ||||
Drug for Ferroptosis | Suppressor | ||||
Response Target | Cystine/glutamate transporter (SLC7A11) | Driver; Suppressor | |||
Responsed Disease | Chronic kidney disease | ICD-11: GB61 | |||
Pathway Response | Ferroptosis | hsa04216 | |||
Fatty acid metabolism | hsa01212 | ||||
Cell Process | Cell ferroptosis | ||||
In Vitro Model |
mPRTECs (Mouse primary renal tubular epithelial cells) | ||||
In Vivo Model |
For UUO-induced CKD, the mice were randomly assigned into four groups (n = 6 per group): UUO, UUO + FN, UUO + VST, and Sham. The mice were anesthetized by intraperitoneal injection of pentobarbital sodium(30 mg/kg). Then, UUO surgery orsham operation was performed as previously described. Mice in the UUO + FN group were orally administrated with 40 mg/kg/day FN (dissolved in 10% DMSO). For positive control, mice in UUO + VST group were orally treated with 20 mg/kg/day VST (dissolved in 10% DMSO). Mice in the UUO and Sham groups were given equivalent solvent by oral. All mice were sacrificed 7 days post-UUO. For UUO-induced CKD, the mice were randomly assigned into four groups (n = 6 per group): UUO, UUO + FN, UUO + VST, and Sham. The mice were anesthetized by intraperitoneal injection of pentobarbital sodium (30 mg/kg). Then, UUO surgery or sham operation was performed as previously described. Mice in the UUO + FN group were orally administrated with 40 mg/kg/day FN (dissolved in 10 % DMSO). For positive control, mice in UUO + VST group were orally treated with 20 mg/kg/day VST (dissolved in 10 % DMSO). Mice in the UUO and Sham groups were given equivalent solvent by oral. All mice were sacrificed 7 days post-UUO.
Click to Show/Hide
|
||||
Response regulation | Formononetin (FN) alleviates chronic kidney disease (CKD) by impeding ferroptosis-associated fibrosis by suppressing the Smad3/ATF3/SLC7A11 signaling and could serve as a candidate therapeutic drug for CKD. In addition, FN also promoted the separation of the Nrf2/Keap1 complex and enhanced Nrf2 nuclear accumulation. | ||||
Tectorigenin
[Investigative]
In total 1 item(s) under this drug | |||||
Experiment 1 Reporting the Ferroptosis-centered Drug Response | [1] | ||||
Drug for Ferroptosis | Suppressor | ||||
Response Target | NADPH oxidase 4 (NOX4) | Driver | |||
Responsed Disease | Unilateral ureteral obstruction | ICD-11: MG30 | |||
Pathway Response | Fatty acid metabolism | hsa01212 | |||
Cell Process | Cell ferroptosis | ||||
In Vitro Model |
mRTECs (Mouse renal tubular epithelial cells) | ||||
In Vivo Model |
The male C57BL/6 mice (8 weeks old, 22-25 g body weight) used in this study were purchased from Dashuo Bio-Technique Co. Ltd. (Chengdu, China) and were maintained in 12 hr of light/12 hr of darkness. The mice were randomly divided into the following 4 groups (n = 8 per group): Sham, UUO, UUO with tectorigenin (20 mg/kg/day, dissolved in saline with 10% dimethyl sulfoxide [DMSO]) or irbesartan (IRB, a positive control, 20 mg/kg/day) treatment. After anesthesia with 1% pentobarbital, the left ureter was exposed through the lower left incision on the midline of the back and blocked by two-point ligation with 40 silk thread as previously described. The Sham-operated mice underwent the same operation but absence of ligation. The tectorigenin and IRB group were administered intraperitoneally with drug daily for 7 consecutive days since surgery. Sham-operated mice and UUO mice were received the equal volume of solvent.
Click to Show/Hide
|
||||
Response regulation | Tectorigenin exerts as a Smad3 inhibitor to suppress Smad3 activation through an Nox4-dependent mechanism. Tectorigenin protects against unilateral ureteral obstruction by inhibiting Smad3-mediated ferroptosis and fibrosis. | ||||
References