Iron articles from across Nature Portfolio

Iron is a growth factor for many microbes, and its availability is critical for the course of infections. A new study uncovers a mechanism by which extracellular vesicles released by macrophages withdraw iron from the blood, thereby limiting iron access for bacteria and improving outcomes from sepsis.

Iron is essential to the production of myocardial energy and proteins critical for cardiovascular function. Nearly 50% of patients with heart failure with reduced ejection fraction (HFrEF) meet current criteria for iron deficiency, and there has been considerable interest in intravenous repletion of iron stores as a therapeutic strategy to improve HFrEF outcomes. However, the data on intravenous iron therapy in HFrEF have been mixed.

Scherer and colleagues demonstrate that manipulation of iron concentrations in the mitochondrial matrix of macrophages has profound effects on their polarization, leading to concomitant changes in adipocyte iron concentrations and, ultimately, systemic metabolic effects.

Living organisms face the dual challenge of acquiring enough iron to perform biological functions while preventing toxic iron accretion. A study now shows that sensing of iron-catalysed free radicals by a druggable gene-regulatory pathway helps the body avoid iron poisoning.

The PIVOTAL trial shows that proactive intravenous (i.v.) iron administration reduces cardiovascular events and deaths, transfusions and erythropoiesis-stimulating agent doses and does not increase infections in patients on haemodialysis. These findings upend the warnings of guidelines and experts about the dangers of i.v. iron and prove that maintaining low iron stores is harmful.