Ferroptosis Regulator Information

General Information of the Ferroptosis Regulator (ID: REG10126)

Regulator Name	Mitogen-activated protein kinase 1 (MAPK1)
Synonyms	ERK2, PRKM1, PRKM2; ERT1; Extracellular signal-regulated kinase 2; MAP kinase isoform p42; Mitogen-activated protein kinase 2 Click to Show/Hide
Gene Name	MAPK1
Gene ID	5594
Regulator Type	Protein coding
Uniprot ID	P28482
Sequence	MAAAAAAGAGPEMVRGQVFDVGPRYTNLSYIGEGAYGMVCSAYDNVNKVRVAIKKISPFE HQTYCQRTLREIKILLRFRHENIIGINDIIRAPTIEQMKDVYIVQDLMETDLYKLLKTQH LSNDHICYFLYQILRGLKYIHSANVLHRDLKPSNLLLNTTCDLKICDFGLARVADPDHDH TGFLTEYVATRWYRAPEIMLNSKGYTKSIDIWSVGCILAEMLSNRPIFPGKHYLDQLNHI LGILGSPSQEDLNCIINLKARNYLLSLPHKNKVPWNRLFPNADSKALDLLDKMLTFNPHK RIEVEQALAHPYLEQYYDPSDEPIAEAPFKFDMELDDLPKEKLKELIFEETARFQPGYRS Click to Show/Hide
Family	CAMK Ser/Thr protein kinase family
Function	Serine/threonine kinase which acts as an essential component of the MAP kinase signal transduction pathway. MAPK1/ERK2 and MAPK3/ERK1 are the 2 MAPKs which play an important role in the MAPK/ERK cascade. They participate also in a signaling cascade initiated by activated KIT and KITLG/SCF. Depending on the cellular context, the MAPK/ERK cascade mediates diverse biological functions such as cell growth, adhesion, survival and differentiation through the regulation of transcription, translation, cytoskeletal rearrangements. The MAPK/ERK cascade also plays a role in initiation and regulation of meiosis, mitosis, and postmitotic functions in differentiated cells by phosphorylating a number of transcription factors. About 160 substrates have already been discovered for ERKs. Many of these substrates are localized in the nucleus, and seem to participate in the regulation of transcription upon stimulation. However, other substrates are found in the cytosol as well as in other cellular organelles, and those are responsible for processes such as translation, mitosis and apoptosis. Moreover, the MAPK/ERK cascade is also involved in the regulation of the endosomal dynamics, including lysosome processing and endosome cycling through the perinuclear recycling compartment (PNRC); as well as in the fragmentation of the Golgi apparatus during mitosis. The substrates include transcription factors (such as ATF2, BCL6, ELK1, ERF, FOS, HSF4 or SPZ1), cytoskeletal elements (such as CANX, CTTN, GJA1, MAP2, MAPT, PXN, SORBS3 or STMN1), regulators of apoptosis (such as BAD, BTG2, CASP9, DAPK1, IER3, MCL1 or PPARG), regulators of translation (such as EIF4EBP1 and FXR1) and a variety of other signaling-related molecules (like ARHGEF2, DCC, FRS2 or GRB10). Protein kinases (such as RAF1, RPS6KA1/RSK1, RPS6KA3/RSK2, RPS6KA2/RSK3, RPS6KA6/RSK4, SYK, MKNK1/MNK1, MKNK2/MNK2, RPS6KA5/MSK1, RPS6KA4/MSK2, MAPKAPK3 or MAPKAPK5) and phosphatases (such as DUSP1, DUSP4, DUSP6 or DUSP16) are other substrates which enable the propagation the MAPK/ERK signal to additional cytosolic and nuclear targets, thereby extending the specificity of the cascade. Mediates phosphorylation of TPR in response to EGF stimulation. May play a role in the spindle assembly checkpoint. Phosphorylates PML and promotes its interaction with PIN1, leading to PML degradation. Phosphorylates CDK2AP2. Click to Show/Hide
HGNC ID	HGNC:6871
KEGG ID	hsa:5594

Full List of the Ferroptosis Target of This Regulator and Corresponding Disease/Drug Response(s)

MAPK1 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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Solute carrier family 40 member 1 (SLC40A1) [Suppressor; Marker]

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	Corpus uteri cancer		ICD-11: 2C76	Disease Info
Responsed Drug	Simvastatin		Investigative	Drug Info
Pathway Response	MAPK signaling pathway			hsa04010
	Ferroptosis			hsa04216
Cell Process	Cell ferroptosis
	Cell proliferation
In Vitro Model	Ishikawa cells	Endometrial adenocarcinoma	Homo sapiens	CVCL_2529
Response regulation	Simvastatin has the potential to be a targeted drug for endometrial cancer (EC) treatment. Besides, the inhibition to the RAS/MAPK signaling pathway allows simvastatin to induce ferroptosis through up-regulating the level of ROS, MDA, Fe2+, and TRF1 (TF) and reducing the level of GSH, SLC7A11, and FPN in cells.

Serotransferrin (TF) [Driver; Suppressor; Marker]

Target Info

In total 1 item(s) under this target
Experiment 1 Reporting the Ferroptosis Target of This Regulator				[1]
Target for Ferroptosis	Marker/Suppressor/Driver
Responsed Disease	Corpus uteri cancer		ICD-11: 2C76	Disease Info
Responsed Drug	Simvastatin		Investigative	Drug Info
Pathway Response	MAPK signaling pathway			hsa04010
	Ferroptosis			hsa04216
Cell Process	Cell ferroptosis
	Cell proliferation
In Vitro Model	Ishikawa cells	Endometrial adenocarcinoma	Homo sapiens	CVCL_2529
Response regulation	Simvastatin has the potential to be a targeted drug for endometrial cancer (EC) treatment. Besides, the inhibition to the RAS/MAPK signaling pathway allows simvastatin to induce ferroptosis through up-regulating the level of ROS, MDA, Fe2+, and TRF1 (TF) and reducing the level of GSH, SLC7A11, and FPN in cells.

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			[2]
Target for Ferroptosis	Suppressor
Responsed Disease	Lung injury	ICD-11: NB32	Disease Info
Responsed Drug	Salidroside	Investigative	Drug Info
Pathway Response	Fatty acid metabolism		hsa01212
	Ferroptosis		hsa04216
Cell Process	Cell ferroptosis
In Vitro Model	mLT (Mouse lung tissue)
In Vivo Model	In our study, the 32 mice were randomly divided for four groups (n = 8 per group): (1) room-air-expose (sham), (2) hyperoxia-expose with Sal (Sal + Hyperoxia), (3) hyperoxia-exposed (Hyperoxia), (4) hyperoxia-exposed with Y-320 (an inhibitor of IL-17) (Y-320 + Hyperoxia). The mice exposed to normoxia groups were placed in room air with 21% oxygen, and the mice exposed to hyperoxia were placed in over 90% oxygen for 24 h. The continue exposure to over 90% oxygen was achieved in a self-made airtight box which attached to a medical oxygen cylinder, and the O2 level inside was continuously monitored with O2 analyzer, mice had free access to food and water. In the first three days before exposure to the hyperoxia, mice in the Sal + Hyperoxia group or Y-320 + Hyperoxia group were treated with Sal (100 mg/Kg) or Y-320 (2 mg/Kg) once orally every day, while the rest of groups were given equal isotonic saline. Based on the above experiments, eight 8-week-old KM mice were randomly divided into two groups: Sal + Hyperoxia group and Sal + Hyperoxia + IL-17A group. Sal + Hyperoxia + IL-17A group, mice were i.v. injected with 50 ug/kg of recombinant mouse IL-17A (210-17, Pepro Tech, USA). Animal were sacrificed following reperfusion, and lungs were stored at -80 until further experimental analysis. Click to Show/Hide
Response regulation	When we applied recombinant IL-17A in Sal+hyperoxia group mice, the protein levels of IL-17RA, Act1, TRAF6, p38 MAPK and p-p38 MAPK increased significantly, and the expression level of GPX4 significantly decreased. Therefore, we demonstrated that IL-17A/IL-17RA mediates ferroptosis of AECII, least in part, via Act1/TRAF6/p38 MAPK pathway, which is responsible for the protective effects of salidroside on hyperoxia-induced acute lung injury (HALI).

Cystine/glutamate transporter (SLC7A11) [Driver; 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	Corpus uteri cancer		ICD-11: 2C76	Disease Info
Responsed Drug	Simvastatin		Investigative	Drug Info
Pathway Response	MAPK signaling pathway			hsa04010
	Ferroptosis			hsa04216
Cell Process	Cell ferroptosis
	Cell proliferation
In Vitro Model	Ishikawa cells	Endometrial adenocarcinoma	Homo sapiens	CVCL_2529
Response regulation	Simvastatin has the potential to be a targeted drug for endometrial cancer (EC) treatment. Besides, the inhibition to the RAS/MAPK signaling pathway allows simvastatin to induce ferroptosis through up-regulating the level of ROS, MDA, Fe2+, and TRF1 (TF) and reducing the level of GSH, SLC7A11, and FPN in cells.

Unspecific Target [Unspecific Target]

In total 1 item(s) under this target
Experiment 1 Reporting the Ferroptosis Target of This Regulator			[3]
Responsed Disease	Acute kidney failure	ICD-11: GB60	Disease Info
Responsed Drug	Loganin	Investigative	Drug Info
Pathway Response	Fatty acid metabolism		hsa01212
	Ferroptosis		hsa04216
	Apoptosis		hsa04210
Cell Process	Cell ferroptosis
	Cell apoptosis
In Vitro Model	mKTs (Mouse knee tissues)
In Vivo Model	All experiments were performed according to the protocols approved by the Animal Care Committee of Wonkwang University. AKI was induced by a single intraperitoneal injection of cisplatin (10 mg/kg). One h before cisplatin injection, mice in the loganin group received 1, 10, or 20 mg/kg of loganin orally, and mice in the U0126 group received 10 mg/kg of U0126 intraperitoneally. They were sacrificed at 72 h after cisplatin injection, and their blood and kidneys were collected. Click to Show/Hide
Response regulation	Histological kidney injury, proximal tubule damages, and renal cell death, such as apoptosis and ferroptosis, were reduced by loganin treatment. Also, pro-inflammatory cytokines, such as interleukin (IL)-1, IL-6, and tumor necrosis factor (TNF)-, reduced by loganin treatment. Furthermore, loganin deactivated the extracellular signal-regulated kinases (ERK) 1 and 2 during acute kidney injury.

Corpus uteri cancer [ICD-11: 2C76]

Disease Info

In total 3 item(s) under this disease
Experiment 1 Reporting the Ferroptosis-centered Disease Response				[1]
Target Regulator	Mitogen-activated protein kinase 1 (MAPK1)		Protein coding	Regulator Info
Responsed Drug	Simvastatin		Investigative	Drug Info
Pathway Response	MAPK signaling pathway			hsa04010
	Ferroptosis			hsa04216
Cell Process	Cell ferroptosis
	Cell proliferation
In Vitro Model	Ishikawa cells	Endometrial adenocarcinoma	Homo sapiens	CVCL_2529
Response regulation	Simvastatin has the potential to be a targeted drug for endometrial cancer (EC) treatment. Besides, the inhibition to the RAS/MAPK signaling pathway allows simvastatin to induce ferroptosis through up-regulating the level of ROS, MDA, Fe2+, and TRF1 (TF) and reducing the level of GSH, SLC7A11, and FPN in cells.
Experiment 2 Reporting the Ferroptosis-centered Disease Response				[1]
Target Regulator	Mitogen-activated protein kinase 1 (MAPK1)		Protein coding	Regulator Info
Responsed Drug	Simvastatin		Investigative	Drug Info
Pathway Response	MAPK signaling pathway			hsa04010
	Ferroptosis			hsa04216
Cell Process	Cell ferroptosis
	Cell proliferation
In Vitro Model	Ishikawa cells	Endometrial adenocarcinoma	Homo sapiens	CVCL_2529
Response regulation	Simvastatin has the potential to be a targeted drug for endometrial cancer (EC) treatment. Besides, the inhibition to the RAS/MAPK signaling pathway allows simvastatin to induce ferroptosis through up-regulating the level of ROS, MDA, Fe2+, and TRF1 (TF) and reducing the level of GSH, SLC7A11, and FPN in cells.
Experiment 3 Reporting the Ferroptosis-centered Disease Response				[1]
Target Regulator	Mitogen-activated protein kinase 1 (MAPK1)		Protein coding	Regulator Info
Responsed Drug	Simvastatin		Investigative	Drug Info
Pathway Response	MAPK signaling pathway			hsa04010
	Ferroptosis			hsa04216
Cell Process	Cell ferroptosis
	Cell proliferation
In Vitro Model	Ishikawa cells	Endometrial adenocarcinoma	Homo sapiens	CVCL_2529
Response regulation	Simvastatin has the potential to be a targeted drug for endometrial cancer (EC) treatment. Besides, the inhibition to the RAS/MAPK signaling pathway allows simvastatin to induce ferroptosis through up-regulating the level of ROS, MDA, Fe2+, and TRF1 (TF) and reducing the level of GSH, SLC7A11, and FPN in cells.

Lung injury [ICD-11: NB32]

Disease Info

In total 1 item(s) under this disease
Experiment 1 Reporting the Ferroptosis-centered Disease Response			[2]
Target Regulator	Mitogen-activated protein kinase 1 (MAPK1)	Protein coding	Regulator Info
Responsed Drug	Salidroside	Investigative	Drug Info
Pathway Response	Fatty acid metabolism		hsa01212
	Ferroptosis		hsa04216
Cell Process	Cell ferroptosis
In Vitro Model	mLT (Mouse lung tissue)
In Vivo Model	In our study, the 32 mice were randomly divided for four groups (n = 8 per group): (1) room-air-expose (sham), (2) hyperoxia-expose with Sal (Sal + Hyperoxia), (3) hyperoxia-exposed (Hyperoxia), (4) hyperoxia-exposed with Y-320 (an inhibitor of IL-17) (Y-320 + Hyperoxia). The mice exposed to normoxia groups were placed in room air with 21% oxygen, and the mice exposed to hyperoxia were placed in over 90% oxygen for 24 h. The continue exposure to over 90% oxygen was achieved in a self-made airtight box which attached to a medical oxygen cylinder, and the O2 level inside was continuously monitored with O2 analyzer, mice had free access to food and water. In the first three days before exposure to the hyperoxia, mice in the Sal + Hyperoxia group or Y-320 + Hyperoxia group were treated with Sal (100 mg/Kg) or Y-320 (2 mg/Kg) once orally every day, while the rest of groups were given equal isotonic saline. Based on the above experiments, eight 8-week-old KM mice were randomly divided into two groups: Sal + Hyperoxia group and Sal + Hyperoxia + IL-17A group. Sal + Hyperoxia + IL-17A group, mice were i.v. injected with 50 ug/kg of recombinant mouse IL-17A (210-17, Pepro Tech, USA). Animal were sacrificed following reperfusion, and lungs were stored at -80 until further experimental analysis. Click to Show/Hide
Response regulation	When we applied recombinant IL-17A in Sal+hyperoxia group mice, the protein levels of IL-17RA, Act1, TRAF6, p38 MAPK and p-p38 MAPK increased significantly, and the expression level of GPX4 significantly decreased. Therefore, we demonstrated that IL-17A/IL-17RA mediates ferroptosis of AECII, least in part, via Act1/TRAF6/p38 MAPK pathway, which is responsible for the protective effects of salidroside on hyperoxia-induced acute lung injury (HALI).

Acute kidney failure [ICD-11: GB60]

Disease Info

In total 1 item(s) under this disease
Experiment 1 Reporting the Ferroptosis-centered Disease Response			[3]
Target Regulator	Mitogen-activated protein kinase 1 (MAPK1)	Protein coding	Regulator Info
Responsed Drug	Loganin	Investigative	Drug Info
Pathway Response	Fatty acid metabolism		hsa01212
	Ferroptosis		hsa04216
	Apoptosis		hsa04210
Cell Process	Cell ferroptosis
	Cell apoptosis
In Vitro Model	mKTs (Mouse knee tissues)
In Vivo Model	All experiments were performed according to the protocols approved by the Animal Care Committee of Wonkwang University. AKI was induced by a single intraperitoneal injection of cisplatin (10 mg/kg). One h before cisplatin injection, mice in the loganin group received 1, 10, or 20 mg/kg of loganin orally, and mice in the U0126 group received 10 mg/kg of U0126 intraperitoneally. They were sacrificed at 72 h after cisplatin injection, and their blood and kidneys were collected. Click to Show/Hide
Response regulation	Histological kidney injury, proximal tubule damages, and renal cell death, such as apoptosis and ferroptosis, were reduced by loganin treatment. Also, pro-inflammatory cytokines, such as interleukin (IL)-1, IL-6, and tumor necrosis factor (TNF)-, reduced by loganin treatment. Furthermore, loganin deactivated the extracellular signal-regulated kinases (ERK) 1 and 2 during acute kidney injury.

Salidroside [Investigative]

Drug Info

In total 1 item(s) under this drug
Experiment 1 Reporting the Ferroptosis-centered Drug Response			[2]
Drug for Ferroptosis	Inducer
Response Target	Phospholipid hydroperoxide glutathione peroxidase (GPX4)	Suppressor	Target Info
Responsed Disease	Lung injury	ICD-11: NB32	Disease Info
Pathway Response	Fatty acid metabolism		hsa01212
	Ferroptosis		hsa04216
Cell Process	Cell ferroptosis
In Vitro Model	mLT (Mouse lung tissue)
In Vivo Model	In our study, the 32 mice were randomly divided for four groups (n = 8 per group): (1) room-air-expose (sham), (2) hyperoxia-expose with Sal (Sal + Hyperoxia), (3) hyperoxia-exposed (Hyperoxia), (4) hyperoxia-exposed with Y-320 (an inhibitor of IL-17) (Y-320 + Hyperoxia). The mice exposed to normoxia groups were placed in room air with 21% oxygen, and the mice exposed to hyperoxia were placed in over 90% oxygen for 24 h. The continue exposure to over 90% oxygen was achieved in a self-made airtight box which attached to a medical oxygen cylinder, and the O2 level inside was continuously monitored with O2 analyzer, mice had free access to food and water. In the first three days before exposure to the hyperoxia, mice in the Sal + Hyperoxia group or Y-320 + Hyperoxia group were treated with Sal (100 mg/Kg) or Y-320 (2 mg/Kg) once orally every day, while the rest of groups were given equal isotonic saline. Based on the above experiments, eight 8-week-old KM mice were randomly divided into two groups: Sal + Hyperoxia group and Sal + Hyperoxia + IL-17A group. Sal + Hyperoxia + IL-17A group, mice were i.v. injected with 50 ug/kg of recombinant mouse IL-17A (210-17, Pepro Tech, USA). Animal were sacrificed following reperfusion, and lungs were stored at -80 until further experimental analysis. Click to Show/Hide
Response regulation	When we applied recombinant IL-17A in Sal+hyperoxia group mice, the protein levels of IL-17RA, Act1, TRAF6, p38 MAPK and p-p38 MAPK increased significantly, and the expression level of GPX4 significantly decreased. Therefore, we demonstrated that IL-17A/IL-17RA mediates ferroptosis of AECII, least in part, via Act1/TRAF6/p38 MAPK pathway, which is responsible for the protective effects of salidroside on hyperoxia-induced acute lung injury (HALI).

Simvastatin [Investigative]

Drug Info

In total 3 item(s) under this drug
Experiment 1 Reporting the Ferroptosis-centered Drug Response				[1]
Drug for Ferroptosis	Inducer
Response Target	Solute carrier family 40 member 1 (SLC40A1)		Suppressor; Marker	Target Info
Responsed Disease	Corpus uteri cancer		ICD-11: 2C76	Disease Info
Pathway Response	MAPK signaling pathway			hsa04010
	Ferroptosis			hsa04216
Cell Process	Cell ferroptosis
	Cell proliferation
In Vitro Model	Ishikawa cells	Endometrial adenocarcinoma	Homo sapiens	CVCL_2529
Response regulation	Simvastatin has the potential to be a targeted drug for endometrial cancer (EC) treatment. Besides, the inhibition to the RAS/MAPK signaling pathway allows simvastatin to induce ferroptosis through up-regulating the level of ROS, MDA, Fe2+, and TRF1 (TF) and reducing the level of GSH, SLC7A11, and FPN in cells.
Experiment 2 Reporting the Ferroptosis-centered Drug Response				[1]
Drug for Ferroptosis	Inducer
Response Target	Serotransferrin (TF)		Driver; Suppressor; Marker	Target Info
Responsed Disease	Corpus uteri cancer		ICD-11: 2C76	Disease Info
Pathway Response	MAPK signaling pathway			hsa04010
	Ferroptosis			hsa04216
Cell Process	Cell ferroptosis
	Cell proliferation
In Vitro Model	Ishikawa cells	Endometrial adenocarcinoma	Homo sapiens	CVCL_2529
Response regulation	Simvastatin has the potential to be a targeted drug for endometrial cancer (EC) treatment. Besides, the inhibition to the RAS/MAPK signaling pathway allows simvastatin to induce ferroptosis through up-regulating the level of ROS, MDA, Fe2+, and TRF1 (TF) and reducing the level of GSH, SLC7A11, and FPN in cells.
Experiment 3 Reporting the Ferroptosis-centered Drug Response				[1]
Drug for Ferroptosis	Inducer
Response Target	Cystine/glutamate transporter (SLC7A11)		Driver; Suppressor	Target Info
Responsed Disease	Corpus uteri cancer		ICD-11: 2C76	Disease Info
Pathway Response	MAPK signaling pathway			hsa04010
	Ferroptosis			hsa04216
Cell Process	Cell ferroptosis
	Cell proliferation
In Vitro Model	Ishikawa cells	Endometrial adenocarcinoma	Homo sapiens	CVCL_2529
Response regulation	Simvastatin has the potential to be a targeted drug for endometrial cancer (EC) treatment. Besides, the inhibition to the RAS/MAPK signaling pathway allows simvastatin to induce ferroptosis through up-regulating the level of ROS, MDA, Fe2+, and TRF1 (TF) and reducing the level of GSH, SLC7A11, and FPN in cells.

Loganin [Investigative]

Drug Info

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	Acute kidney failure	ICD-11: GB60	Disease Info
Pathway Response	Fatty acid metabolism		hsa01212
	Ferroptosis		hsa04216
	Apoptosis		hsa04210
Cell Process	Cell ferroptosis
	Cell apoptosis
In Vitro Model	mKTs (Mouse knee tissues)
In Vivo Model	All experiments were performed according to the protocols approved by the Animal Care Committee of Wonkwang University. AKI was induced by a single intraperitoneal injection of cisplatin (10 mg/kg). One h before cisplatin injection, mice in the loganin group received 1, 10, or 20 mg/kg of loganin orally, and mice in the U0126 group received 10 mg/kg of U0126 intraperitoneally. They were sacrificed at 72 h after cisplatin injection, and their blood and kidneys were collected. Click to Show/Hide
Response regulation	Histological kidney injury, proximal tubule damages, and renal cell death, such as apoptosis and ferroptosis, were reduced by loganin treatment. Also, pro-inflammatory cytokines, such as interleukin (IL)-1, IL-6, and tumor necrosis factor (TNF)-, reduced by loganin treatment. Furthermore, loganin deactivated the extracellular signal-regulated kinases (ERK) 1 and 2 during acute kidney injury.

References

Ref 1	Simvastatin Inhibits Endometrial Cancer Malignant Behaviors by Suppressing RAS/Mitogen-Activated Protein Kinase (MAPK) Pathway-Mediated Reactive Oxygen Species (ROS) and Ferroptosis. Evid Based Complement Alternat Med. 2022 Oct 14;2022:6177477. doi: 10.1155/2022/6177477. eCollection 2022.
Ref 2	Salidroside attenuates HALI via IL-17A-mediated ferroptosis of alveolar epithelial cells by regulating Act1-TRAF6-p38 MAPK pathway. Cell Commun Signal. 2022 Nov 21;20(1):183. doi: 10.1186/s12964-022-00994-1.
Ref 3	Loganin Attenuates the Severity of Acute Kidney Injury Induced by Cisplatin through the Inhibition of ERK Activation in Mice. Int J Mol Sci. 2021 Jan 31;22(3):1421. doi: 10.3390/ijms22031421.

Ferroptosis Regulator Information

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Correspondence

Prof. Shuiping Liu