Ferroptosis Regulator Information

General Information of the Ferroptosis Regulator (ID: REG10271)
Regulator Name Ferritin, mitochondrial (FTMT)
Gene Name FTMT
Gene ID 94033
Regulator Type Protein coding
Uniprot ID Q8N4E7
Sequence
MLSCFRLLSRHISPSLASLRPVRCCFALPLRWAPGRPLDPRQIAPRRPLAAAASSRDPTG
PAAGPSRVRQNFHPDSEAAINRQINLELYASYVYLSMAYYFSRDDVALNNFSRYFLHQSR
EETEHAEKLMRLQNQRGGRIRLQDIKKPEQDDWESGLHAMECALLLEKNVNQSLLELHAL
ASDKGDPHLCDFLETYYLNEQVKSIKELGDHVHNLVKMGAPDAGLAEYLFDTHTLGNENK
QN

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Family Ferritin family
Function
Catalyzes the oxidation of ferrous iron(II) to ferric iron(III) and stores iron in a soluble, non-toxic, readily available form. Important for iron homeostasis. Iron is taken up in the ferrous form and deposited as ferric hydroxides after oxidation.

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HGNC ID
HGNC:17345
KEGG ID hsa:94033
Full List of the Ferroptosis Target of This Regulator and Corresponding Disease/Drug Response(s)
FTMT 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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Phospholipid hydroperoxide glutathione peroxidase (GPX4) [Suppressor]
 Target Info 
In total 1 item(s) under this target
Experiment 1 Reporting the Ferroptosis Target of This Regulator [1]
Target for Ferroptosis Suppressor
Responsed Disease Osteoporosis ICD-11: FB83
 Disease Info 
Responsed Drug Carbonyl cyanide-m-chlorophenyl-hydrazine Investigative
 Drug Info 
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Autophagy hsa04140
Cell Process Cell ferroptosis
Cell autophagy
In Vitro Model
 hFOB 1.19 cells Normal Homo sapiens CVCL_3708
In Vivo Model
Forty-five SD rats (3 months old, 200 ± 20 g) were obtained from the Department of Experimental Animals in China Medical University (Animal Certificate Number: SCXK (Liaoning) 2008-0005). Fifteen rats grew as control while other thirty rats were established T2DOP model. The model rats were given a high-fat feed and 12 h/day water for 2 months. Then streptozotocin was intraperitoneally injected at 30 mg/kg. Seventy-two hours later, the model was successfully established when insulin sensitivity index decreased and fasting plasma glucose exceeded 7.8 mmol/L. Then all rats continue grew 3 months to cause osteoporosis. Thirty model rats were divided into two groups. One was fifteen T2DOP rats only, and other was fifteen T2DOP rats with deferoxamine (DFO) treatment (60 mg/kg/day, intraperitoneally inject, last for the last 1 month).

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Response regulation Carbonyl cyanide-m-chlorophenyl-hydrazine (CCCP) is a mitophagy agonist. Through adding mitophagy agonist CCCP to osteoblasts, we found the increase of ROS and lipid peroxidation while GPX4 decreased. FtMt inhibited the occurrence of ferroptosis in osteoblasts by reducing oxidative stress caused by excess ferrous ions, and FtMt deficiency induced mitophagy in the pathogenesis of type 2 diabetic osteoporosis (T2DOP).
Unspecific Target [Unspecific Target]
In total 1 item(s) under this target
Experiment 1 Reporting the Ferroptosis Target of This Regulator [2]
Responsed Disease Fibrosarcoma ICD-11: 2B53
 Disease Info 
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Autophagy hsa04140
Cell Process Cell ferroptosis
Cell autophagy
In Vitro Model
 HT-1080 cells Fibrosarcoma Homo sapiens CVCL_0317
Response regulation Reduced NCOA4 expression resulted from a lower rate of hypoxic NCOA4 transcription combined with a micro RNA 6862-5p-dependent degradation of NCOA4 mRNA, the latter being regulated by c-jun N-terminal kinase (JNK). Pharmacological inhibition of JNK under hypoxia increased NCOA4 and prevented FTMT induction in fibrosarcoma HT1080 cells.
Osteoporosis [ICD-11: FB83]
 Disease Info 
In total 1 item(s) under this disease
Experiment 1 Reporting the Ferroptosis-centered Disease Response [1]
Target Regulator Ferritin, mitochondrial (FTMT) Protein coding
 Regulator Info 
Responsed Drug Carbonyl cyanide-m-chlorophenyl-hydrazine Investigative
 Drug Info 
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Autophagy hsa04140
Cell Process Cell ferroptosis
Cell autophagy
In Vitro Model
 hFOB 1.19 cells Normal Homo sapiens CVCL_3708
In Vivo Model
Forty-five SD rats (3 months old, 200 ± 20 g) were obtained from the Department of Experimental Animals in China Medical University (Animal Certificate Number: SCXK (Liaoning) 2008-0005). Fifteen rats grew as control while other thirty rats were established T2DOP model. The model rats were given a high-fat feed and 12 h/day water for 2 months. Then streptozotocin was intraperitoneally injected at 30 mg/kg. Seventy-two hours later, the model was successfully established when insulin sensitivity index decreased and fasting plasma glucose exceeded 7.8 mmol/L. Then all rats continue grew 3 months to cause osteoporosis. Thirty model rats were divided into two groups. One was fifteen T2DOP rats only, and other was fifteen T2DOP rats with deferoxamine (DFO) treatment (60 mg/kg/day, intraperitoneally inject, last for the last 1 month).

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Response regulation Carbonyl cyanide-m-chlorophenyl-hydrazine (CCCP) is a mitophagy agonist. Through adding mitophagy agonist CCCP to osteoblasts, we found the increase of ROS and lipid peroxidation while GPX4 decreased. FtMt inhibited the occurrence of ferroptosis in osteoblasts by reducing oxidative stress caused by excess ferrous ions, and FtMt deficiency induced mitophagy in the pathogenesis of type 2 diabetic osteoporosis (T2DOP).
Fibrosarcoma [ICD-11: 2B53]
 Disease Info 
In total 1 item(s) under this disease
Experiment 1 Reporting the Ferroptosis-centered Disease Response [2]
Target Regulator Ferritin, mitochondrial (FTMT) Protein coding
 Regulator Info 
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Autophagy hsa04140
Cell Process Cell ferroptosis
Cell autophagy
In Vitro Model
 HT-1080 cells Fibrosarcoma Homo sapiens CVCL_0317
Response regulation Reduced NCOA4 expression resulted from a lower rate of hypoxic NCOA4 transcription combined with a micro RNA 6862-5p-dependent degradation of NCOA4 mRNA, the latter being regulated by c-jun N-terminal kinase (JNK). Pharmacological inhibition of JNK under hypoxia increased NCOA4 and prevented FTMT induction in fibrosarcoma HT1080 cells.
Carbonyl cyanide-m-chlorophenyl-hydrazine [Investigative]
 Drug Info 
In total 1 item(s) under this drug
Experiment 1 Reporting the Ferroptosis-centered Drug Response [1]
Drug for Ferroptosis Inducer
Response Target Phospholipid hydroperoxide glutathione peroxidase (GPX4) Suppressor
 Target Info 
Responsed Disease Osteoporosis ICD-11: FB83
 Disease Info 
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Autophagy hsa04140
Cell Process Cell ferroptosis
Cell autophagy
In Vitro Model
 hFOB 1.19 cells Normal Homo sapiens CVCL_3708
In Vivo Model
Forty-five SD rats (3 months old, 200 ± 20 g) were obtained from the Department of Experimental Animals in China Medical University (Animal Certificate Number: SCXK (Liaoning) 2008-0005). Fifteen rats grew as control while other thirty rats were established T2DOP model. The model rats were given a high-fat feed and 12 h/day water for 2 months. Then streptozotocin was intraperitoneally injected at 30 mg/kg. Seventy-two hours later, the model was successfully established when insulin sensitivity index decreased and fasting plasma glucose exceeded 7.8 mmol/L. Then all rats continue grew 3 months to cause osteoporosis. Thirty model rats were divided into two groups. One was fifteen T2DOP rats only, and other was fifteen T2DOP rats with deferoxamine (DFO) treatment (60 mg/kg/day, intraperitoneally inject, last for the last 1 month).

    Click to Show/Hide
Response regulation Carbonyl cyanide-m-chlorophenyl-hydrazine (CCCP) is a mitophagy agonist. Through adding mitophagy agonist CCCP to osteoblasts, we found the increase of ROS and lipid peroxidation while GPX4 decreased. FtMt inhibited the occurrence of ferroptosis in osteoblasts by reducing oxidative stress caused by excess ferrous ions, and FtMt deficiency induced mitophagy in the pathogenesis of type 2 diabetic osteoporosis (T2DOP).
References
Ref 1 Mitochondrial Ferritin Deficiency Promotes Osteoblastic Ferroptosis Via Mitophagy in Type 2 Diabetic Osteoporosis. Biol Trace Elem Res. 2022 Jan;200(1):298-307. doi: 10.1007/s12011-021-02627-z. Epub 2021 Feb 16.
Ref 2 Hypoxia inhibits ferritinophagy, increases mitochondrial ferritin, and protects from ferroptosis. Redox Biol. 2020 Sep;36:101670. doi: 10.1016/j.redox.2020.101670. Epub 2020 Aug 3.