New insights into the role of iron in inflammation and atherosclerosis

Abstract

Iron is fundamental for life-essential processes. However, it can also cause oxidative damage, which is thought to trigger numerous pathologies, including cardiovascular diseases. The role of iron in the pathogenesis of atherosclerosis is still not completely understood. Macrophages are both key players in the handling of iron throughout the body and in the onset, progression and destabilization of atherosclerotic plaques. Iron itself might impact atherosclerosis through its effects on macrophages. However, while targeting iron metabolism within macrophages may have some beneficial effects on preventing atherosclerotic plaque progression there may also be negative consequences. Thus, the prevailing view of iron being capable of accelerating the progression of coronary disease through lipid peroxidation may not fully take into account the multi-faceted role of iron in pathogenesis of atherosclerosis. In this review, we will summarize the current understanding of iron metabolism in the context of the complex interplay between iron, inflammation, and atherosclerosis.

Regulation of tissue iron homeostasis: the macrophage “ferrostat”

“…Furthermore, in atherosclerosis, Hb-handling Mɸs have been reported to take on both pro-and antiatherogenic roles (reviewed in ref. 142). Thus, there seems to be a complex temporal relationship between iron trafficking and disease pathogenicity.…”

MicroRNA-183-5p acts as a potential diagnostic biomarker for atherosclerosis and regulates the growth of vascular smooth muscle cell

“…AS is a chronic inflammatory and metabolic disease, and is the main causes of cardiovascular diseases [16]. Although great progress has been made in understanding AS development, deaths from AS is still high.…”

Iron Metabolism, Ferroptosis, and the Links With Alzheimer’s Disease

“…And FPN1is controlled by the iron-regulatory hormone hepcidin, which is mainly synthesized and secreted by hepatocytes (Ganz, 2013). Hepcidin binds directly to FPN1 and triggers its internalization, ubiquitination, and degradation (Sangkhae and Nemeth, 2017;Cornelissen et al, 2019). Ultimately, iron across the BBB can be absorbed by neurons, microglia, and astrocytes via the same iron metabolism-related proteins (McCarthy and Kosman, 2015;Simpson et al, 2015;Bu et al, 2019;Yan and Zhang, 2019).…”