Ferroptosis Regulator Information

General Information of the Ferroptosis Regulator (ID: REG20103)
Regulator Name rno-miR-23a-3p (miRNA)
Synonyms
rno-miR-23a-3p
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Gene Name rno-miR-23a-3p
Regulator Type miRNA
MiRBase ID MIMAT0000792
Full List of the Ferroptosis Target of This Regulator and Corresponding Disease/Drug Response(s)
rno-miR-23a-3p 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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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 Supraventricular tachycardia ICD-11: BC81
 Disease Info 
Responsed Drug GW4869 Investigative
 Drug Info 
Pathway Response Ferroptosis hsa04216
Cell Process Cell ferroptosis
In Vitro Model
 CHO-S/H9C2 cells Normal Cricetulus griseus CVCL_A0TS
rCFs (Rat cardiac fibroblasts)
In Vivo Model
Eighteen beagles, randomly divided into three groups, both sexes and an average age of 1 year, weighing 7.5 ± 1.5 kg, were used for the study as follows: Sham group (n = 6), Pacing group (n = 6), and GW4869 + Pacing group (n = 6). Each beagle canine was given an intramuscular injection of 25 mg/kg ketamine sulfate before being premedicated with pentobarbital sodium (30 mg/kg, intravenous injection) and ventilated with room air by a respirator (MAO01746, Harvard Apparatus Holliston, United States). Venous access was established to supply saline (50-100 mL/h) or pentobarbital sodium (2.5 mg/kg/h).

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Response regulation The exosome inhibitor GW4869 reduced ferroptosis, fibrosis, and inflammation and improved histological and electrophysiological remodeling. Pacing-CF-exos highly expressed miR-23a-3p by informatics analysis and experimental verification. Inhibitor- miR-23a-3p protected h9c2 cells from ferroptosis accompanying with upregulation of SLC7A11. The development of atrial fibrillation (AF) in a persistent direction could be prevented by intervening with exosomal miRNAs to reduce oxidative stress injury and ferroptosis.
Nuclear factor erythroid 2-related factor 2 (NFE2L2) [Suppressor; Marker]
 Target Info 
In total 1 item(s) under this target
Experiment 1 Reporting the Ferroptosis Target of This Regulator [2]
Target for Ferroptosis Marker/Suppressor
Responsed Disease Intracerebral hemorrhage ICD-11: 8B00
 Disease Info 
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Cell Process Cell ferroptosis
In Vitro Model
 rNCs (Rat neuronal cells)
hBCs (Brain cells)
In Vivo Model
Male 8-week-old Sprague-Dawley rats were chosen for this study. These animals were randomized to 3, 4, or 5 groups: Design for 3 groups: Sham group, rats underwent sham operation; ICH group, rats underwent ICH operation; ICH + Ac group, rats underwent ICH operation and treated with acupuncture at target acupoints. Design for 4 groups: Sham group; ICH group; ICH + Ac group; ICH + sAc group, rats underwent ICH operation and treated with acupuncture at non-acupoints located 1 cm posterior and parallel to Baihui-penetrating-Qubin needling as previously described. Another design for 4 groups: Sham group; ICH group; ICH + NC group, rats underwent ICH operation and injected with antagomiR-NC; ICH + antagomiR group, rats underwent ICH operation and injected with antagomiR-23a-3p.

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Response regulation Acupuncture alleviated ferroptosis and decreased miR-23a-3p expression, as evidenced by the increased NFE2L2 nuclear translocation and expressions of heme oxygenase-1 and glutathione peroxidase 4 and the decreased iron and malondialdehyde contents and reactive oxygen species accumulation. Notably, the binding site of miR-23a-3p existed in NFE2L2. Taken together, acupuncture may alleviate the neuronal cell death, inflammation, and ferroptosis after intracerebral hemorrhage (ICH) by down-regulating miR-23a-3p.
Supraventricular tachycardia [ICD-11: BC81]
 Disease Info 
In total 1 item(s) under this disease
Experiment 1 Reporting the Ferroptosis-centered Disease Response [1]
Target Regulator rno-miR-23a-3p (miRNA) miRNA
 Regulator Info 
Responsed Drug GW4869 Investigative
 Drug Info 
Pathway Response Ferroptosis hsa04216
Cell Process Cell ferroptosis
In Vitro Model
 CHO-S/H9C2 cells Normal Cricetulus griseus CVCL_A0TS
rCFs (Rat cardiac fibroblasts)
In Vivo Model
Eighteen beagles, randomly divided into three groups, both sexes and an average age of 1 year, weighing 7.5 ± 1.5 kg, were used for the study as follows: Sham group (n = 6), Pacing group (n = 6), and GW4869 + Pacing group (n = 6). Each beagle canine was given an intramuscular injection of 25 mg/kg ketamine sulfate before being premedicated with pentobarbital sodium (30 mg/kg, intravenous injection) and ventilated with room air by a respirator (MAO01746, Harvard Apparatus Holliston, United States). Venous access was established to supply saline (50-100 mL/h) or pentobarbital sodium (2.5 mg/kg/h).

    Click to Show/Hide
Response regulation The exosome inhibitor GW4869 reduced ferroptosis, fibrosis, and inflammation and improved histological and electrophysiological remodeling. Pacing-CF-exos highly expressed miR-23a-3p by informatics analysis and experimental verification. Inhibitor- miR-23a-3p protected h9c2 cells from ferroptosis accompanying with upregulation of SLC7A11. The development of atrial fibrillation (AF) in a persistent direction could be prevented by intervening with exosomal miRNAs to reduce oxidative stress injury and ferroptosis.
Intracerebral hemorrhage [ICD-11: 8B00]
 Disease Info 
In total 1 item(s) under this disease
Experiment 1 Reporting the Ferroptosis-centered Disease Response [2]
Target Regulator rno-miR-23a-3p (miRNA) miRNA
 Regulator Info 
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Cell Process Cell ferroptosis
In Vitro Model
 rNCs (Rat neuronal cells)
hBCs (Brain cells)
In Vivo Model
Male 8-week-old Sprague-Dawley rats were chosen for this study. These animals were randomized to 3, 4, or 5 groups: Design for 3 groups: Sham group, rats underwent sham operation; ICH group, rats underwent ICH operation; ICH + Ac group, rats underwent ICH operation and treated with acupuncture at target acupoints. Design for 4 groups: Sham group; ICH group; ICH + Ac group; ICH + sAc group, rats underwent ICH operation and treated with acupuncture at non-acupoints located 1 cm posterior and parallel to Baihui-penetrating-Qubin needling as previously described. Another design for 4 groups: Sham group; ICH group; ICH + NC group, rats underwent ICH operation and injected with antagomiR-NC; ICH + antagomiR group, rats underwent ICH operation and injected with antagomiR-23a-3p.

    Click to Show/Hide
Response regulation Acupuncture alleviated ferroptosis and decreased miR-23a-3p expression, as evidenced by the increased NFE2L2 nuclear translocation and expressions of heme oxygenase-1 and glutathione peroxidase 4 and the decreased iron and malondialdehyde contents and reactive oxygen species accumulation. Notably, the binding site of miR-23a-3p existed in NFE2L2. Taken together, acupuncture may alleviate the neuronal cell death, inflammation, and ferroptosis after intracerebral hemorrhage (ICH) by down-regulating miR-23a-3p.
GW4869 [Investigative]
 Drug Info 
In total 1 item(s) under this drug
Experiment 1 Reporting the Ferroptosis-centered Drug Response [1]
Drug for Ferroptosis Suppressor
Response Target Cystine/glutamate transporter (SLC7A11) Driver; Suppressor
 Target Info 
Responsed Disease Supraventricular tachycardia ICD-11: BC81
 Disease Info 
Pathway Response Ferroptosis hsa04216
Cell Process Cell ferroptosis
In Vitro Model
 CHO-S/H9C2 cells Normal Cricetulus griseus CVCL_A0TS
rCFs (Rat cardiac fibroblasts)
In Vivo Model
Eighteen beagles, randomly divided into three groups, both sexes and an average age of 1 year, weighing 7.5 ± 1.5 kg, were used for the study as follows: Sham group (n = 6), Pacing group (n = 6), and GW4869 + Pacing group (n = 6). Each beagle canine was given an intramuscular injection of 25 mg/kg ketamine sulfate before being premedicated with pentobarbital sodium (30 mg/kg, intravenous injection) and ventilated with room air by a respirator (MAO01746, Harvard Apparatus Holliston, United States). Venous access was established to supply saline (50-100 mL/h) or pentobarbital sodium (2.5 mg/kg/h).

    Click to Show/Hide
Response regulation The exosome inhibitor GW4869 reduced ferroptosis, fibrosis, and inflammation and improved histological and electrophysiological remodeling. Pacing-CF-exos highly expressed miR-23a-3p by informatics analysis and experimental verification. Inhibitor- miR-23a-3p protected h9c2 cells from ferroptosis accompanying with upregulation of SLC7A11. The development of atrial fibrillation (AF) in a persistent direction could be prevented by intervening with exosomal miRNAs to reduce oxidative stress injury and ferroptosis.
References
Ref 1 Cardiac Fibroblasts Promote Ferroptosis in Atrial Fibrillation by Secreting Exo-miR-23a-3p Targeting SLC7A11. Oxid Med Cell Longev. 2022 May 29;2022:3961495. doi: 10.1155/2022/3961495. eCollection 2022.
Ref 2 Acupuncture Ameliorates Neuronal Cell Death, Inflammation, and Ferroptosis and Downregulated miR-23a-3p After Intracerebral Hemorrhage in Rats. J Mol Neurosci. 2021 Sep;71(9):1863-1875. doi: 10.1007/s12031-020-01770-x. Epub 2021 Jan 5.