Emerging roles of ferroptosis in infectious diseases

In living organisms, lipid peroxidation is a continuously occurring cellular process and therefore involved in various physiological and pathological contexts. Among the broad variety of lipids, polyunsaturated fatty acids (PUFA) constitute a major target of oxygenation either when released as mediators by phospholipases or when present in membranous phospholipids. The last decade has seen the characterization of an iron- and lipid peroxidation-dependent cell necrosis, namely, ferroptosis, that involves the accumulation of peroxidized PUFA-containing phospholipids. Further studies could link ferroptosis in a very large body of (physio)-pathological processes, including cancer, neurodegenerative, and metabolic diseases. In this review, we mostly focus on the emerging involvement of lipid peroxidation-driven ferroptosis in infectious diseases, and the immune consequences. We also discuss the putative ability of microbial virulence factors to exploit or to dampen ferroptosis regulatory pathways to their own benefit.

Automated summary

Lipid peroxidation is a continuously occurring cellular process in living organisms, affecting various physiological and pathological contexts. Polyunsaturated fatty acids are a major target of oxidation, especially in membranous phospholipids. Recent studies have identified ferroptosis as an iron- and lipid peroxidation-dependent cell necrosis, with implications in a wide range of physiological and pathological processes, such as cancer, neurodegenerative diseases, and metabolic disorders.