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Journal Article Research Support, Non-U.S. Gov't Review Ppublish 34 citations

PubMed: 34263712 DOI: 10.1080/1744666X.2021.1953981

Pathological mechanisms of abnormal iron metabolism and mitochondrial dysfunction in systemic lupus erythematosus.

Expert Rev Clin Immunol 17(9):957-967

Authors: Chris Wincup, Natalie Sawford, Anisur Rahman

Affiliations

  • Department of Rheumatology, Division of Medicine, University College London, London, UK.

Abstract

Systemic lupus erythematosus [SLE] is a chronic, autoimmune condition characterized by the formation of autoantibodies directed against nuclear components and by oxidative stress. Recently, a number of studies have demonstrated the essential role of iron in the immune response and there is growing evidence that abnormal iron homeostasis can occur in the chronic inflammatory state seen in SLE. Not only is iron vital for hematopoiesis, it is also important for a number of other key physiological processes, in particular in maintaining healthy mitochondrial function. In this review, we highlight the latest understanding with regards to how patients with SLE may be at risk of cellular iron depletion as a result of both absolute and functional iron deficiency. Furthermore, we aim to explain the latest evidence of mitochondrial dysfunction in the pathogenesis of the disease. Growing evidence suggests that both abnormal iron homeostasis and subsequent mitochondrial dysfunction can impair effector immune cell function. Through a greater understanding of these abnormalities, therapeutic options that directly target iron and mitochondria may ultimately represent novel treatment targets that may translate into clinical care of patients with SLE in the near future.

MeSH

Cells, Homeostasis, Mitochondria, Lupus Erythematosus, Systemic, Immune System Diseases, Therapeutics

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