Ferroptosis Regulator Information
General Information of the Ferroptosis Regulator (ID: REG10340)
Full List of the Ferroptosis Target of This Regulator and Corresponding Disease/Drug Response(s)
MAP1LC3A
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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Nuclear receptor coactivator 4 (NCOA4) [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 | Pulmonary fibrosis | ICD-11: CB03 | |||
Responsed Drug | Dihydroquercetin | Preclinical | |||
Pathway Response | Fatty acid metabolism | hsa01212 | |||
Autophagy | hsa04140 | ||||
Cell Process | Cell ferroptosis | ||||
Cell autophagy | |||||
In Vitro Model |
hBEs (Human bronchial epithelial cells) | ||||
MRC-5 cells | Normal | Homo sapiens | CVCL_0440 | ||
In Vivo Model |
Eight-week-old male C57BL/6 mice were purchased from Hubei University of Medicine (Shiyan, China). The SiO2-induced mouse pulmonary fibrosis model was performed. In brief, each group of mice was anesthetized with 1% pentobarbital sodium intraperitoneally at 40 mg/kg body weight and their tracheae had been surgically exposed. In addition, SiO2 suspension (20 mg in 50 ul saline) was instilled in the mice. The vehicle control groups were given an equivalent amount of 0.9% sterile saline. After one week of acclimation, mice were divided randomly into four groups (n = 8 per group). Control group, SiO2 group, SiO2 and low dose of DHQ group (DHQ-L, 10 mg/kg) as well as large dose of DHQ group (DHQ-H, 50 mg/kg).
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Response regulation | Dihydroquercetin suppressed ferritinophagy by down-regulation of microtubule-associated protein 1A/ 1B-light chain 3 (LC3), and up-regulation of ferritin heavy chain 1 (FTH1), nuclear receptor co-activator 4 (NCOA4) in activated HBE cells. Research revealed that inhibition of ferritinophagy-mediated HBE cells ferroptosis was responsible for DHQ to ameliorate SiO2-induced lung fibrosis. | ||||
Ferritin heavy chain (FTH1) [Suppressor; Marker]
In total 1 item(s) under this target | |||||
Experiment 1 Reporting the Ferroptosis Target of This Regulator | [1] | ||||
Target for Ferroptosis | Marker/Suppressor | ||||
Responsed Disease | Pulmonary fibrosis | ICD-11: CB03 | |||
Responsed Drug | Dihydroquercetin | Preclinical | |||
Pathway Response | Fatty acid metabolism | hsa01212 | |||
Autophagy | hsa04140 | ||||
Cell Process | Cell ferroptosis | ||||
Cell autophagy | |||||
In Vitro Model |
hBEs (Human bronchial epithelial cells) | ||||
MRC-5 cells | Normal | Homo sapiens | CVCL_0440 | ||
In Vivo Model |
Eight-week-old male C57BL/6 mice were purchased from Hubei University of Medicine (Shiyan, China). The SiO2-induced mouse pulmonary fibrosis model was performed. In brief, each group of mice was anesthetized with 1% pentobarbital sodium intraperitoneally at 40 mg/kg body weight and their tracheae had been surgically exposed. In addition, SiO2 suspension (20 mg in 50 ul saline) was instilled in the mice. The vehicle control groups were given an equivalent amount of 0.9% sterile saline. After one week of acclimation, mice were divided randomly into four groups (n = 8 per group). Control group, SiO2 group, SiO2 and low dose of DHQ group (DHQ-L, 10 mg/kg) as well as large dose of DHQ group (DHQ-H, 50 mg/kg).
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|
||||
Response regulation | Dihydroquercetin suppressed ferritinophagy by down-regulation of microtubule-associated protein 1A/ 1B-light chain 3 (LC3), and up-regulation of ferritin heavy chain 1 (FTH1), nuclear receptor co-activator 4 (NCOA4) in activated HBE cells. Research revealed that inhibition of ferritinophagy-mediated HBE cells ferroptosis was responsible for DHQ to ameliorate SiO2-induced lung fibrosis. | ||||
Unspecific Target [Unspecific Target]
In total 2 item(s) under this target | |||||
Experiment 1 Reporting the Ferroptosis Target of This Regulator | [2] | ||||
Responsed Disease | Liver fibrosis | ICD-11: DB93 | |||
Responsed Drug | Artesunate | Investigative | |||
Pathway Response | Fatty acid metabolism | hsa01212 | |||
Autophagy | hsa04140 | ||||
Cell Process | Cell ferroptosis | ||||
Cell autophagy | |||||
In Vitro Model |
hHSCs (Human hepatic stellate cells) | ||||
hHSCs (Human hepatic stellate cells) | |||||
In Vivo Model |
6-8-week-old, 20 ± 2 g, male ICR mice, obtained from Nanjing Medical University (Nanjing, China), were randomly divided into five groups (n = 8 per group). Mouse model of chronic liver fibrosis was established by 10% carbon tetrachloride (CCl4, 0.5 ml/100 g body weight) injection. Groups are follows: (1) Control group was intraperitoneally (i.p.) injected with olive oil; (2) Model group was i.p. injected with 10% CCl4 every other day a week for 8 weeks; (3) Low-dose artesunate treatment groups were i.p. injected by CCl4 every other day a week for 8 weeks and daily i.p. injected by 50 mg/kg artesunate for last 4 weeks; (4) Middle-dose artesunate treatment groups were i.p. injected by CCl4 every other day a week for 8 weeks and daily i.p. injected by 100 mg/kg artesunate for last 4 weeks; (5) High-dose artesunate treatment groups were i.p. injected by CCl4 every other day a week for 8 weeks and daily i.p. injected by 200 mg/kg artesunate for last 4 weeks.
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||||
Response regulation | Artesunate evidently triggered ferritinophagy accompanied by up-regulation of LC3 (microtubule-associated protein light chain 3), Atg3, Atg5, Atg6/beclin1, Atg12 (autophagy related genes) and down-regulation of p62, FTH1 (ferritin heavy chain), NCOA4 (nuclear receptor co-activator 4) in activated HSCs. These results suggested that ferritinophagy-mediated HSC ferroptosis was responsible for artesunate-induced anti-fibrosis efficacy in liver fibrosis. | ||||
Experiment 2 Reporting the Ferroptosis Target of This Regulator | [3] | ||||
Responsed Disease | Traumatic brain injury | ICD-11: NA07 | |||
Responsed Drug | Baicalin | Terminated | |||
Pathway Response | Ferroptosis | hsa04216 | |||
Cell Process | Cell ferroptosis | ||||
Cell autophagy | |||||
Cell apoptosis | |||||
In Vitro Model |
rPNs (Rat primary neurons) | ||||
In Vivo Model |
Rats were injected with 4 mL/kg of chloral hydrate for anesthesia and then put on a stereotactic apparatus. Subsequently, the needle was tilted at 55 in the sagittal plane and fixed anterior to the bregma (7.5 mm). The needle tip was toward the right and lowered the anterior to the chiasma (2 mm). Finally, the nonheparinized autologous femoral arterial blood (0.3 mL) was injected into a prechiasmatic cistern using a syringe pump. Rat temperature was maintained at 37 ± 0.5 during the surgery. The rats in the sham group were injected with the same dose of saline into a prechiasmatic cistern. At last, rats were monitored for recovery and then returned to cages.
Click to Show/Hide
|
||||
Response regulation | Baicalin was confirmed to suppress the beclin1, LC3-II, and LC3-I protein levels in rat brain tissues. Moreover, we found that baicalin inhibited neuronal apoptosis. Overall, baicalin suppressed autophagy-dependent ferroptosis in early brain injury after subarachnoid hemorrhage. | ||||
Pulmonary fibrosis [ICD-11: CB03]
In total 2 item(s) under this disease | |||||
Experiment 1 Reporting the Ferroptosis-centered Disease Response | [1] | ||||
Target Regulator | Microtubule-associated proteins 1A/1B light chain 3A (MAP1LC3A) | Protein coding | |||
Responsed Drug | Dihydroquercetin | Preclinical | |||
Pathway Response | Fatty acid metabolism | hsa01212 | |||
Autophagy | hsa04140 | ||||
Cell Process | Cell ferroptosis | ||||
Cell autophagy | |||||
In Vitro Model |
hBEs (Human bronchial epithelial cells) | ||||
MRC-5 cells | Normal | Homo sapiens | CVCL_0440 | ||
In Vivo Model |
Eight-week-old male C57BL/6 mice were purchased from Hubei University of Medicine (Shiyan, China). The SiO2-induced mouse pulmonary fibrosis model was performed. In brief, each group of mice was anesthetized with 1% pentobarbital sodium intraperitoneally at 40 mg/kg body weight and their tracheae had been surgically exposed. In addition, SiO2 suspension (20 mg in 50 ul saline) was instilled in the mice. The vehicle control groups were given an equivalent amount of 0.9% sterile saline. After one week of acclimation, mice were divided randomly into four groups (n = 8 per group). Control group, SiO2 group, SiO2 and low dose of DHQ group (DHQ-L, 10 mg/kg) as well as large dose of DHQ group (DHQ-H, 50 mg/kg).
Click to Show/Hide
|
||||
Response regulation | Dihydroquercetin suppressed ferritinophagy by down-regulation of microtubule-associated protein 1A/ 1B-light chain 3 (LC3), and up-regulation of ferritin heavy chain 1 (FTH1), nuclear receptor co-activator 4 (NCOA4) in activated HBE cells. Research revealed that inhibition of ferritinophagy-mediated HBE cells ferroptosis was responsible for DHQ to ameliorate SiO2-induced lung fibrosis. | ||||
Experiment 2 Reporting the Ferroptosis-centered Disease Response | [1] | ||||
Target Regulator | Microtubule-associated proteins 1A/1B light chain 3A (MAP1LC3A) | Protein coding | |||
Responsed Drug | Dihydroquercetin | Preclinical | |||
Pathway Response | Fatty acid metabolism | hsa01212 | |||
Autophagy | hsa04140 | ||||
Cell Process | Cell ferroptosis | ||||
Cell autophagy | |||||
In Vitro Model |
hBEs (Human bronchial epithelial cells) | ||||
MRC-5 cells | Normal | Homo sapiens | CVCL_0440 | ||
In Vivo Model |
Eight-week-old male C57BL/6 mice were purchased from Hubei University of Medicine (Shiyan, China). The SiO2-induced mouse pulmonary fibrosis model was performed. In brief, each group of mice was anesthetized with 1% pentobarbital sodium intraperitoneally at 40 mg/kg body weight and their tracheae had been surgically exposed. In addition, SiO2 suspension (20 mg in 50 ul saline) was instilled in the mice. The vehicle control groups were given an equivalent amount of 0.9% sterile saline. After one week of acclimation, mice were divided randomly into four groups (n = 8 per group). Control group, SiO2 group, SiO2 and low dose of DHQ group (DHQ-L, 10 mg/kg) as well as large dose of DHQ group (DHQ-H, 50 mg/kg).
Click to Show/Hide
|
||||
Response regulation | Dihydroquercetin suppressed ferritinophagy by down-regulation of microtubule-associated protein 1A/ 1B-light chain 3 (LC3), and up-regulation of ferritin heavy chain 1 (FTH1), nuclear receptor co-activator 4 (NCOA4) in activated HBE cells. Research revealed that inhibition of ferritinophagy-mediated HBE cells ferroptosis was responsible for DHQ to ameliorate SiO2-induced lung fibrosis. | ||||
Liver fibrosis [ICD-11: DB93]
In total 1 item(s) under this disease | |||||
Experiment 1 Reporting the Ferroptosis-centered Disease Response | [2] | ||||
Target Regulator | Microtubule-associated proteins 1A/1B light chain 3A (MAP1LC3A) | Protein coding | |||
Responsed Drug | Artesunate | Investigative | |||
Pathway Response | Fatty acid metabolism | hsa01212 | |||
Autophagy | hsa04140 | ||||
Cell Process | Cell ferroptosis | ||||
Cell autophagy | |||||
In Vitro Model |
hHSCs (Human hepatic stellate cells) | ||||
hHSCs (Human hepatic stellate cells) | |||||
In Vivo Model |
6-8-week-old, 20 ± 2 g, male ICR mice, obtained from Nanjing Medical University (Nanjing, China), were randomly divided into five groups (n = 8 per group). Mouse model of chronic liver fibrosis was established by 10% carbon tetrachloride (CCl4, 0.5 ml/100 g body weight) injection. Groups are follows: (1) Control group was intraperitoneally (i.p.) injected with olive oil; (2) Model group was i.p. injected with 10% CCl4 every other day a week for 8 weeks; (3) Low-dose artesunate treatment groups were i.p. injected by CCl4 every other day a week for 8 weeks and daily i.p. injected by 50 mg/kg artesunate for last 4 weeks; (4) Middle-dose artesunate treatment groups were i.p. injected by CCl4 every other day a week for 8 weeks and daily i.p. injected by 100 mg/kg artesunate for last 4 weeks; (5) High-dose artesunate treatment groups were i.p. injected by CCl4 every other day a week for 8 weeks and daily i.p. injected by 200 mg/kg artesunate for last 4 weeks.
Click to Show/Hide
|
||||
Response regulation | Artesunate evidently triggered ferritinophagy accompanied by up-regulation of LC3 (microtubule-associated protein light chain 3), Atg3, Atg5, Atg6/beclin1, Atg12 (autophagy related genes) and down-regulation of p62, FTH1 (ferritin heavy chain), NCOA4 (nuclear receptor co-activator 4) in activated HSCs. These results suggested that ferritinophagy-mediated HSC ferroptosis was responsible for artesunate-induced anti-fibrosis efficacy in liver fibrosis. | ||||
Traumatic brain injury [ICD-11: NA07]
In total 1 item(s) under this disease | |||||
Experiment 1 Reporting the Ferroptosis-centered Disease Response | [3] | ||||
Target Regulator | Microtubule-associated proteins 1A/1B light chain 3A (MAP1LC3A) | Protein coding | |||
Responsed Drug | Baicalin | Terminated | |||
Pathway Response | Ferroptosis | hsa04216 | |||
Cell Process | Cell ferroptosis | ||||
Cell autophagy | |||||
Cell apoptosis | |||||
In Vitro Model |
rPNs (Rat primary neurons) | ||||
In Vivo Model |
Rats were injected with 4 mL/kg of chloral hydrate for anesthesia and then put on a stereotactic apparatus. Subsequently, the needle was tilted at 55 in the sagittal plane and fixed anterior to the bregma (7.5 mm). The needle tip was toward the right and lowered the anterior to the chiasma (2 mm). Finally, the nonheparinized autologous femoral arterial blood (0.3 mL) was injected into a prechiasmatic cistern using a syringe pump. Rat temperature was maintained at 37 ± 0.5 during the surgery. The rats in the sham group were injected with the same dose of saline into a prechiasmatic cistern. At last, rats were monitored for recovery and then returned to cages.
Click to Show/Hide
|
||||
Response regulation | Baicalin was confirmed to suppress the beclin1, LC3-II, and LC3-I protein levels in rat brain tissues. Moreover, we found that baicalin inhibited neuronal apoptosis. Overall, baicalin suppressed autophagy-dependent ferroptosis in early brain injury after subarachnoid hemorrhage. | ||||
Dihydroquercetin
[Preclinical]
In total 2 item(s) under this drug | |||||
Experiment 1 Reporting the Ferroptosis-centered Drug Response | [1] | ||||
Drug for Ferroptosis | Suppressor | ||||
Response Target | Nuclear receptor coactivator 4 (NCOA4) | Driver | |||
Responsed Disease | Pulmonary fibrosis | ICD-11: CB03 | |||
Pathway Response | Fatty acid metabolism | hsa01212 | |||
Autophagy | hsa04140 | ||||
Cell Process | Cell ferroptosis | ||||
Cell autophagy | |||||
In Vitro Model |
hBEs (Human bronchial epithelial cells) | ||||
MRC-5 cells | Normal | Homo sapiens | CVCL_0440 | ||
In Vivo Model |
Eight-week-old male C57BL/6 mice were purchased from Hubei University of Medicine (Shiyan, China). The SiO2-induced mouse pulmonary fibrosis model was performed. In brief, each group of mice was anesthetized with 1% pentobarbital sodium intraperitoneally at 40 mg/kg body weight and their tracheae had been surgically exposed. In addition, SiO2 suspension (20 mg in 50 ul saline) was instilled in the mice. The vehicle control groups were given an equivalent amount of 0.9% sterile saline. After one week of acclimation, mice were divided randomly into four groups (n = 8 per group). Control group, SiO2 group, SiO2 and low dose of DHQ group (DHQ-L, 10 mg/kg) as well as large dose of DHQ group (DHQ-H, 50 mg/kg).
Click to Show/Hide
|
||||
Response regulation | Dihydroquercetin suppressed ferritinophagy by down-regulation of microtubule-associated protein 1A/ 1B-light chain 3 (LC3), and up-regulation of ferritin heavy chain 1 (FTH1), nuclear receptor co-activator 4 (NCOA4) in activated HBE cells. Research revealed that inhibition of ferritinophagy-mediated HBE cells ferroptosis was responsible for DHQ to ameliorate SiO2-induced lung fibrosis. | ||||
Experiment 2 Reporting the Ferroptosis-centered Drug Response | [1] | ||||
Drug for Ferroptosis | Suppressor | ||||
Response Target | Ferritin heavy chain (FTH1) | Suppressor; Marker | |||
Responsed Disease | Pulmonary fibrosis | ICD-11: CB03 | |||
Pathway Response | Fatty acid metabolism | hsa01212 | |||
Autophagy | hsa04140 | ||||
Cell Process | Cell ferroptosis | ||||
Cell autophagy | |||||
In Vitro Model |
hBEs (Human bronchial epithelial cells) | ||||
MRC-5 cells | Normal | Homo sapiens | CVCL_0440 | ||
In Vivo Model |
Eight-week-old male C57BL/6 mice were purchased from Hubei University of Medicine (Shiyan, China). The SiO2-induced mouse pulmonary fibrosis model was performed. In brief, each group of mice was anesthetized with 1% pentobarbital sodium intraperitoneally at 40 mg/kg body weight and their tracheae had been surgically exposed. In addition, SiO2 suspension (20 mg in 50 ul saline) was instilled in the mice. The vehicle control groups were given an equivalent amount of 0.9% sterile saline. After one week of acclimation, mice were divided randomly into four groups (n = 8 per group). Control group, SiO2 group, SiO2 and low dose of DHQ group (DHQ-L, 10 mg/kg) as well as large dose of DHQ group (DHQ-H, 50 mg/kg).
Click to Show/Hide
|
||||
Response regulation | Dihydroquercetin suppressed ferritinophagy by down-regulation of microtubule-associated protein 1A/ 1B-light chain 3 (LC3), and up-regulation of ferritin heavy chain 1 (FTH1), nuclear receptor co-activator 4 (NCOA4) in activated HBE cells. Research revealed that inhibition of ferritinophagy-mediated HBE cells ferroptosis was responsible for DHQ to ameliorate SiO2-induced lung fibrosis. | ||||
Baicalin
[Terminated]
In total 1 item(s) under this drug | |||||
Experiment 1 Reporting the Ferroptosis-centered Drug Response | [3] | ||||
Drug for Ferroptosis | Suppressor | ||||
Response Target | Unspecific Target | ||||
Responsed Disease | Traumatic brain injury | ICD-11: NA07 | |||
Pathway Response | Ferroptosis | hsa04216 | |||
Cell Process | Cell ferroptosis | ||||
Cell autophagy | |||||
Cell apoptosis | |||||
In Vitro Model |
rPNs (Rat primary neurons) | ||||
In Vivo Model |
Rats were injected with 4 mL/kg of chloral hydrate for anesthesia and then put on a stereotactic apparatus. Subsequently, the needle was tilted at 55 in the sagittal plane and fixed anterior to the bregma (7.5 mm). The needle tip was toward the right and lowered the anterior to the chiasma (2 mm). Finally, the nonheparinized autologous femoral arterial blood (0.3 mL) was injected into a prechiasmatic cistern using a syringe pump. Rat temperature was maintained at 37 ± 0.5 during the surgery. The rats in the sham group were injected with the same dose of saline into a prechiasmatic cistern. At last, rats were monitored for recovery and then returned to cages.
Click to Show/Hide
|
||||
Response regulation | Baicalin was confirmed to suppress the beclin1, LC3-II, and LC3-I protein levels in rat brain tissues. Moreover, we found that baicalin inhibited neuronal apoptosis. Overall, baicalin suppressed autophagy-dependent ferroptosis in early brain injury after subarachnoid hemorrhage. | ||||
Artesunate
[Investigative]
In total 1 item(s) under this drug | |||||
Experiment 1 Reporting the Ferroptosis-centered Drug Response | [2] | ||||
Drug for Ferroptosis | Inducer | ||||
Response Target | Unspecific Target | ||||
Responsed Disease | Liver fibrosis | ICD-11: DB93 | |||
Pathway Response | Fatty acid metabolism | hsa01212 | |||
Autophagy | hsa04140 | ||||
Cell Process | Cell ferroptosis | ||||
Cell autophagy | |||||
In Vitro Model |
hHSCs (Human hepatic stellate cells) | ||||
hHSCs (Human hepatic stellate cells) | |||||
In Vivo Model |
6-8-week-old, 20 ± 2 g, male ICR mice, obtained from Nanjing Medical University (Nanjing, China), were randomly divided into five groups (n = 8 per group). Mouse model of chronic liver fibrosis was established by 10% carbon tetrachloride (CCl4, 0.5 ml/100 g body weight) injection. Groups are follows: (1) Control group was intraperitoneally (i.p.) injected with olive oil; (2) Model group was i.p. injected with 10% CCl4 every other day a week for 8 weeks; (3) Low-dose artesunate treatment groups were i.p. injected by CCl4 every other day a week for 8 weeks and daily i.p. injected by 50 mg/kg artesunate for last 4 weeks; (4) Middle-dose artesunate treatment groups were i.p. injected by CCl4 every other day a week for 8 weeks and daily i.p. injected by 100 mg/kg artesunate for last 4 weeks; (5) High-dose artesunate treatment groups were i.p. injected by CCl4 every other day a week for 8 weeks and daily i.p. injected by 200 mg/kg artesunate for last 4 weeks.
Click to Show/Hide
|
||||
Response regulation | Artesunate evidently triggered ferritinophagy accompanied by up-regulation of LC3 (microtubule-associated protein light chain 3), Atg3, Atg5, Atg6/beclin1, Atg12 (autophagy related genes) and down-regulation of p62, FTH1 (ferritin heavy chain), NCOA4 (nuclear receptor co-activator 4) in activated HSCs. These results suggested that ferritinophagy-mediated HSC ferroptosis was responsible for artesunate-induced anti-fibrosis efficacy in liver fibrosis. | ||||
References