Ferroptosis-centered Disease Response Information

General Information of the Disease (ID: DIS00101)
Name
Aortic aneurysm
ICD
ICD-11: BD50
Full List of Target(s) of This Ferroptosis-centered Disease
Prostaglandin G/H synthase 2 (PTGS2)
 Target Info 
In total 2 item(s) under this target
Experiment 1 Reporting the Ferroptosis-centered Disease Response by This Target [1]
Target for Ferroptosis Marker
Responsed Disease Aortic aneurysm [ICD-11: BD50]
Responsed Drug Acrolein Investigative
 Drug Info 
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Cell Process Cell ferroptosis
In Vitro Model rVSMCs (Rat vascular smooth muscle cells)
A7r5 cells Normal Rattus norvegicus CVCL_0137
EAhy926 cells Normal Homo sapiens CVCL_3901
C3H/10T1/2 cells Normal Mus musculus CVCL_0190
In Vivo Model
C57BL/6J wild-type mice (8-10 wk old, male) were purchased from Japan SLC (Tokyo, Japan). Mice were housed (4/cage, RAIR HD-ventilated micro-isolator animal housing systems; Laboratory Products, Seaford, DE) in an environment maintained at 23 ± 2 with ad libitum access to food and water under a 12-h:12-h light-dark cycle, with lights on from 0800 to 2000. A total of 13 mice were used. The aorta was harvested immediately after mice were euthanized by inhalation of carbon dioxide, washed in 0.1% antibiotics/PBS, and cut into 3-4-mm rings. The aortic rings were cultured in 10% FCS/DMEM for 3 h and then treated with CSE (0.8 mg/mL) for the indicated periods.

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Response regulation VSMC ferroptosis was induced by acrolein and methyl vinyl ketone, major constituents of CSE. CSE also induced the upregulation of Ptgs2 mRNA, lipid peroxidation, and intracellular GSH depletion, which are key features of ferroptosis. These findings suggest that ferroptosis is a potential therapeutic target for preventing aortic aneurysm and dissection.
Experiment 2 Reporting the Ferroptosis-centered Disease Response by This Target [1]
Target for Ferroptosis Marker
Responsed Disease Aortic aneurysm [ICD-11: BD50]
Responsed Drug Methyl vinyl ketone Investigative
 Drug Info 
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Cell Process Cell ferroptosis
In Vitro Model rVSMCs (Rat vascular smooth muscle cells)
A7r5 cells Normal Rattus norvegicus CVCL_0137
EAhy926 cells Normal Homo sapiens CVCL_3901
C3H/10T1/2 cells Normal Mus musculus CVCL_0190
In Vivo Model
C57BL/6J wild-type mice (8-10 wk old, male) were purchased from Japan SLC (Tokyo, Japan). Mice were housed (4/cage, RAIR HD-ventilated micro-isolator animal housing systems; Laboratory Products, Seaford, DE) in an environment maintained at 23 ± 2 with ad libitum access to food and water under a 12-h:12-h light-dark cycle, with lights on from 0800 to 2000. A total of 13 mice were used. The aorta was harvested immediately after mice were euthanized by inhalation of carbon dioxide, washed in 0.1% antibiotics/PBS, and cut into 3-4-mm rings. The aortic rings were cultured in 10% FCS/DMEM for 3 h and then treated with CSE (0.8 mg/mL) for the indicated periods.

    Click to Show/Hide
Response regulation VSMC ferroptosis was induced by acrolein and methyl vinyl ketone, major constituents of CSE. CSE also induced the upregulation of Ptgs2 mRNA, lipid peroxidation, and intracellular GSH depletion, which are key features of ferroptosis. These findings suggest that ferroptosis is a potential therapeutic target for preventing aortic aneurysm and dissection.
References
Ref 1 Cigarette smoke extract induces ferroptosis in vascular smooth muscle cells. Am J Physiol Heart Circ Physiol. 2020 Mar 1;318(3):H508-H518. doi: 10.1152/ajpheart.00559.2019. Epub 2020 Jan 24.