Abstract
Ferroptosis is a unique form of programmed cell death driven by iron-dependent phospholipid peroxidation that was proposed in recent years. It plays an important role in processes of various trace element-related diseases and is regulated by redox homeostasis and various cellular metabolic pathways (iron, amino acids, lipids, sugars), as well as disease-related signaling pathways. Some limited pioneering studies have demonstrated ferroptosis as a mechanism for the health effects of essential trace elements and potentially toxic trace elements, with crosstalk among them. The aim of this review is to bring together research articles and identify key direct and indirect evidence regarding essential trace elements (iron, selenium, zinc, copper, chromium, manganese) and potentially toxic trace elements (arsenic, aluminum, mercury) and their possible roles in ferroptosis. Our review may help determine future research priorities and opportunities.
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