Links Between Iron and Lipids: Implications in Some Major Human Diseases

Maintenance of iron homeostasis is critical to cellular health as both its excess and insufficiency are detrimental. Likewise, lipids, which are essential components of cellular membranes and signaling mediators, must also be tightly regulated to hinder disease progression. Recent research, using a...

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Published inPharmaceuticals (Basel, Switzerland) Vol. 11; no. 4; p. 113
Main Authors Rockfield, Stephanie, Chhabra, Ravneet, Robertson, Michelle, Rehman, Nabila, Bisht, Richa, Nanjundan, Meera
Format Journal Article
LanguageEnglish
Published Switzerland MDPI AG 22.10.2018
MDPI
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Summary:Maintenance of iron homeostasis is critical to cellular health as both its excess and insufficiency are detrimental. Likewise, lipids, which are essential components of cellular membranes and signaling mediators, must also be tightly regulated to hinder disease progression. Recent research, using a myriad of model organisms, as well as data from clinical studies, has revealed links between these two metabolic pathways, but the mechanisms behind these interactions and the role these have in the progression of human diseases remains unclear. In this review, we summarize literature describing cross-talk between iron and lipid pathways, including alterations in cholesterol, sphingolipid, and lipid droplet metabolism in response to changes in iron levels. We discuss human diseases correlating with both iron and lipid alterations, including neurodegenerative disorders, and the available evidence regarding the potential mechanisms underlying how iron may promote disease pathogenesis. Finally, we review research regarding iron reduction techniques and their therapeutic potential in treating patients with these debilitating conditions. We propose that iron-mediated alterations in lipid metabolic pathways are involved in the progression of these diseases, but further research is direly needed to elucidate the mechanisms involved.
Bibliography:ObjectType-Article-2
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ISSN:1424-8247
1424-8247
DOI:10.3390/ph11040113