Ferroptosis Regulator Information
General Information of the Ferroptosis Regulator (ID: REG20081)
Full List of the Ferroptosis Target of This Regulator and Corresponding Disease/Drug Response(s)
mmu-miR-33-5p
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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Stearoyl-CoA desaturase (SCD) [Suppressor]
| In total 1 item(s) under this target | |||||
| Experiment 1 Reporting the Ferroptosis Target of This Regulator | [1] | ||||
| Target for Ferroptosis | Suppressor | ||||
| Responsed Disease | Nonalcoholic fatty liver disease | ICD-11: DB92 | |||
| Responsed Drug | D-(-)-Fructose | Investigative | |||
| Pathway Response | Fatty acid metabolism | hsa01212 | |||
| Ferroptosis | hsa04216 | ||||
| Glutathione metabolism | hsa00480 | ||||
| Cell Process | Cell ferroptosis | ||||
In Vitro Model |
hLCs (Liver cells) | ||||
| In Vivo Model |
Four-week-old male and female C57BL/6N mice were obtained from the Central Lab Animal Inc. (Seoul, South Korea) and housed in 42 x 27 x 15 cm polycarbonate cages (six mice per cage). The animals were assigned into either the control group (n = 12; six mice per sex) or fructose intervention group (n = 12; six mice per sex). After a week of acclimation, the fructose group was subjected to 34% fructose in deionized water (wt:vol) over six weeks to induce NAFLD conditions as previously described.11 To note, compared to conventional sugary beverages (e.g., soft drinks), the supplementation level of fructose is higher (11% vs. 34%) to induce liver damage markers within a reasonable intervention time range (i.e., 6 weeks).
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| Response regulation | The protein expressions of SREBP1 and its downstream targets ACC1, FASN and SCD1 were all increased in fructose-treated AML12 hepatocytes, which demonstrates fructose mediated upregulation of SREBP1. MiR-33-5p (miR-33) was identified as the key miRNA responsible for SREBP1 regulation upon fructose intake, which was validated by in vitro transfection assay. Collectively, fructose-induced oxidative damage induces ferroptosis, and miR-33 could be used as a serological biomarker of fructose-induced non-alcoholic fatty liver disease (NAFLD). | ||||
Nonalcoholic fatty liver disease [ICD-11: DB92]
| In total 1 item(s) under this disease | |||||
| Experiment 1 Reporting the Ferroptosis-centered Disease Response | [1] | ||||
| Target Regulator | mmu-miR-33-5p (miRNA) | miRNA | |||
| Responsed Drug | D-(-)-Fructose | Investigative | |||
| Pathway Response | Fatty acid metabolism | hsa01212 | |||
| Ferroptosis | hsa04216 | ||||
| Glutathione metabolism | hsa00480 | ||||
| Cell Process | Cell ferroptosis | ||||
In Vitro Model |
hLCs (Liver cells) | ||||
| In Vivo Model |
Four-week-old male and female C57BL/6N mice were obtained from the Central Lab Animal Inc. (Seoul, South Korea) and housed in 42 x 27 x 15 cm polycarbonate cages (six mice per cage). The animals were assigned into either the control group (n = 12; six mice per sex) or fructose intervention group (n = 12; six mice per sex). After a week of acclimation, the fructose group was subjected to 34% fructose in deionized water (wt:vol) over six weeks to induce NAFLD conditions as previously described.11 To note, compared to conventional sugary beverages (e.g., soft drinks), the supplementation level of fructose is higher (11% vs. 34%) to induce liver damage markers within a reasonable intervention time range (i.e., 6 weeks).
Click to Show/Hide
|
||||
| Response regulation | The protein expressions of SREBP1 and its downstream targets ACC1, FASN and SCD1 were all increased in fructose-treated AML12 hepatocytes, which demonstrates fructose mediated upregulation of SREBP1. MiR-33-5p (miR-33) was identified as the key miRNA responsible for SREBP1 regulation upon fructose intake, which was validated by in vitro transfection assay. Collectively, fructose-induced oxidative damage induces ferroptosis, and miR-33 could be used as a serological biomarker of fructose-induced non-alcoholic fatty liver disease (NAFLD). | ||||
D-(-)-Fructose
[Investigative]
| In total 1 item(s) under this drug | |||||
| Experiment 1 Reporting the Ferroptosis-centered Drug Response | [1] | ||||
| Drug for Ferroptosis | Inducer | ||||
| Response Target | Stearoyl-CoA desaturase (SCD) | Suppressor | |||
| Responsed Disease | Nonalcoholic fatty liver disease | ICD-11: DB92 | |||
| Pathway Response | Fatty acid metabolism | hsa01212 | |||
| Ferroptosis | hsa04216 | ||||
| Glutathione metabolism | hsa00480 | ||||
| Cell Process | Cell ferroptosis | ||||
In Vitro Model |
hLCs (Liver cells) | ||||
| In Vivo Model |
Four-week-old male and female C57BL/6N mice were obtained from the Central Lab Animal Inc. (Seoul, South Korea) and housed in 42 x 27 x 15 cm polycarbonate cages (six mice per cage). The animals were assigned into either the control group (n = 12; six mice per sex) or fructose intervention group (n = 12; six mice per sex). After a week of acclimation, the fructose group was subjected to 34% fructose in deionized water (wt:vol) over six weeks to induce NAFLD conditions as previously described.11 To note, compared to conventional sugary beverages (e.g., soft drinks), the supplementation level of fructose is higher (11% vs. 34%) to induce liver damage markers within a reasonable intervention time range (i.e., 6 weeks).
Click to Show/Hide
|
||||
| Response regulation | The protein expressions of SREBP1 and its downstream targets ACC1, FASN and SCD1 were all increased in fructose-treated AML12 hepatocytes, which demonstrates fructose mediated upregulation of SREBP1. MiR-33-5p (miR-33) was identified as the key miRNA responsible for SREBP1 regulation upon fructose intake, which was validated by in vitro transfection assay. Collectively, fructose-induced oxidative damage induces ferroptosis, and miR-33 could be used as a serological biomarker of fructose-induced non-alcoholic fatty liver disease (NAFLD). | ||||