Exploration of the Role of Ferroptosis in Stroke

The specific hallmark of ferroptosis is the atrophy of mitochondria, while the nucleus remains intact. It is a specific form of cell death. There are few studies on the interaction between ferroptosis and stroke, which greatly hinders our understanding of stroke. Based on the current studies, we need to further explore the relationship between ferroptosis and stroke. With this in mind, Ace Therapeutics offers a comprehensive service to explore the mechanisms of ferroptosis regulation during a stroke. We provide the genomics research platform, proteomics research platform, and metabolomics research platform for screening key biomarkers of different pathways related to ferroptosis. What's more, we offer different stroke models to explore the role of ferroptosis in stroke.

Exploration of the Role of Iron Metabolism in Ferroptosis in Stroke

Iron overload is a key cause of ferroptosis after stroke, which increases mitochondrial oxidative damage and infarct volume. The balance of iron influx and iron efflux maintains the homeostasis of iron metabolism. To explore the role of iron metabolism in ferroptosis in stroke, we provide a complete service.

• We establish in vitro and in vivo animal models of abnormal iron metabolism by drug administration or genetic manipulation.
• For oxidative damage, we offer a variety of protein assays and biochemical testing services.
• For iron metabolism-related proteins, such as TF, TFR1, DMT1, FT, and FPN1, we quantify and localize the proteins by western blotting, immunohistochemistry, ELISA, and immunofluorescence assays.

Exploration of the Role of Amino Acid Metabolism in Ferroptosis in Stroke

Inhibition of the amino acid antiporter system Xc^- leads to a decrease in GSH and GPX4 activity, lipid peroxidation, and ultimately to ferroptosis. Ace Therapeutics provides a mature technology platform to explore the role of amino acid metabolism in ferroptosis in stroke.

• We establish in vitro and in vivo experimental models that affect the function of system Xc- through drug administration to explore the role of system Xc- on ferroptosis in stroke.
• We establish in vitro and in vivo models of abnormal expression of GSH, GPX4, and other proteins by drug administration and genetic manipulation to explore the effect of these proteins on ferroptosis in stroke.

Exploration of the Role of Lipid Peroxidation Metabolism in Ferroptosis in Stroke

Lipid peroxidation is a key step in ferroptosis. Some lipids are subject to peroxidation catalyzed by LOX or induced by ·OH produced in the Fenton reaction; the resulting lipid peroxides can attack proximal PUFAs, which triggers a chain reaction and leads to ferroptosis. In addition, studies have confirmed the ability of 5-LOX to produce toxic lipids that induce ferroptosis. For the role of lipid peroxidation in ferroptosis in stroke, Ace Therapeutics provides relevant experimental models and assays.

• In vitro and in vivo models related to lipid peroxidation are established to explore its role in the pathological process of ferroptosis.
• For the process of lipid peroxidation, we provide a metabolomics assay platform to determine the specific mechanism of action of lipid peroxidation in the pathology of ferroptosis.

Ace Therapeutics offers a one-stop scientific service to explore the role of ferroptosis in stroke in a scientific and accurate manner. If you would like to learn more about our services, please feel free to contact us.

1. Zhang, Y., et al., Ferroptosis and its multifaceted roles in cerebral stroke. Front Cell Neurosci, 2021. 15: p. 615372.
2. Bu, Z. Q., et al., Emerging role of ferroptosis in the pathogenesis of ischemic stroke: A new therapeutic target? ASN Neuro, 2021. 13: p. 17590914211037505.