TABLE 2.

Pharmacological research progress on ferroptosis in ischemic stroke.

Characteristics	Regulations	Reagents and mechanisms
Morphological characteristics: Mitochondrial volume decreases, membrane density increases, and mitochondria decrease or disappear	Positive regulators: ACSL4, Hmox1, NCOA4	Inducers	Mechanism
		Erastin	Inactivates and decreases the level of GSH.
		RSL3	Inactivates GPX4 and causes accumulation of lipid hydroperoxides
		Inhibitors
		Deferoxamine	As an iron chelator, it can prevent iron-dependent lipid peroxidation
		Liproxstatin-1	Inhibits mitochondrial lipid peroxidation and restores the expression of GSH, GPX4 and FSP1
Biochemical characteristics: Ferroptosis is manifested as GSH depletion, GXP4 inactivation, and lipid peroxide accumulation	Negative regulators: GPX4, Nrf2, HSPB1, SLC7A11, FSP1	Selenium	Protects GPX4 and upregulates GPX4 expression
		Ferrostatin-1	Prevents glutamate-induced neurotoxicity and inhibits lipid peroxidation
		Ceruloplasmin	Oxidizes ferrous ions to less toxic ferric forms
		N-Acetylcysteine (NAC)	Maintains intracellular GSH level and lower endogenous oxidant level
		Vitamin D	An antioxidant and a regulator of iron metabolism
		Vitamin E	inhibits LOX activity by competing at the substrate-binding site and by scavenging hydroxyl group radicals