Long-held beliefs that the hardening of the arteries involved in atherosclerosis is linked to the body's iron levels may be unfounded, according to new research from UCLA.
Common thinking is that the greater risk of atherosclerosis in men and post-menopausal women compared to pre-menopausal women is related to higher levels of iron in the body in both groups, the study's lead author Professor Elizabeta Nemeth remarked.
Under this 'iron hypothesis' it is believed the iron-regulatory hormone hepcidin causes the build-up of iron in plaque macrophages - which leads to oxidative stress and inflammation and contributes to atherosclerosis.
However, the new study by Nemeth and her team showed little evidence to support the theory, as the progression of atherosclerosis in animals exposed to excessive iron levels in the macrophage cells was no different than in those with normal iron counts.
Writing in Cell Reports, the team also revealed that there was no increase in the level of hepcidin in the mice at any stage of atherosclerosis progression.
Léon Kautz, first author on the study, branded the lack of evidence for either iron's link with atherosclerosis, or atherosclerosis influence on hepcidin a 'surprise', but conceded the study needs to be replicated in humans to see if the same is true.
Other research groups have started to study hepcidin in atherosclerosis patients, Nemeth noted. A further question raised by her team's study is whether lowering iron beyond normal levels could have a positive effect over atherosclerosis.
"Understanding risk factors for atherosclerosis progression is important for better prevention and treatment of the disease," Nemeth added.
Source: Cell Reports
Published online ahead of print, DOI: 10.1016/j.celrep.2013.11.009
"Testing the Iron Hypothesis in a Mouse Model of Atherosclerosis"
Authors: Leon Kautz, Victoria Gabayan et al.