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Mitochondrial Dysfunction in Autoimmune Diseases

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Immunology".

Deadline for manuscript submissions: 30 April 2024 | Viewed by 1912

Special Issue Editor


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Guest Editor
The Arthritis and Clinical Immunology Program, Oklahoma Medical Research Foundation, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, USA
Interests: systemic lupus erythematosus; Sjögren’s syndrome; prolidase deficiency; free radical biology; experimental urolithiasis; curcumin and other curcuminoids; dietary supplements; microgravity
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Special Issue Information

Dear Colleagues,

Organ-specific autoimmune diseases (type 1 diabetes, thyroiditis, myasthenia gravis, primary biliary cirrhosis, multiple sclerosis, Goodpasture’s syndrome) or systemic autoimmunity (rheumatoid arthritis, progressive systemic sclerosis, systemic lupus erythematosus (SLE), Sjögren’s disease (SjD)) result from the abrogation of self-tolerance. Autoantibodies are characteristic of most of these diseases and are present several years before the diagnosis of SLE or SjD and serve as markers for future diseases. The precise involvement of cellular organelles concerning the etiology of inflammation in autoimmune diseases has not been fully explored. Mitochondrial dysfunction occurs in many of these diseases. Fatigue and other symptoms occur in most chronic diseases when an imbalance between biogenesis and mitophagy leads to progressive pathological conditions linked to mitochondrial dysfunction.

In this Special Issue of IJMS, we are looking for articles that delineate the molecular mechanisms mediating the pathological conditions of autoimmune diseases. This request would include articles that provide insights into molecular aspects of the initiation and progression of the disease by glandular, vascular endothelial cells, environmental triggers, cytokine activation of lymphocytes, the apoptosis of glandular cells, free radical-mediated oxidative damage, imbalance between mitochondrial biogenesis and mitophagy, mitochondrial structural changes, and mitochondrial dysfunction. We also welcome review papers in these areas and articles describing novel therapeutic targets and biomarkers.

Dr. Biji Theyilamannil Kurien
Guest Editor

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Keywords

  • autoimmune diseases
  • autoantibodies
  • autophagy
  • mitophagy
  • mitochondrial hyperpolarization
  • mitochondrial dysfunction
  • oxidative phosphorylation
  • oxidative damage
  • fatigue
  • chronic inflammation

Published Papers (1 paper)

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Review

18 pages, 674 KiB  
Review
Coenzyme Q10 and Autoimmune Disorders: An Overview
by David Mantle and Iain P. Hargreaves
Int. J. Mol. Sci. 2024, 25(8), 4576; https://doi.org/10.3390/ijms25084576 - 22 Apr 2024
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Abstract
Some 90 autoimmune disorders have been described in medical literature, affecting most of the tissues within the body. Autoimmune disorders may be difficult to treat, and there is a need to develop novel therapeutic strategies for these disorders. Autoimmune disorders are characterised by [...] Read more.
Some 90 autoimmune disorders have been described in medical literature, affecting most of the tissues within the body. Autoimmune disorders may be difficult to treat, and there is a need to develop novel therapeutic strategies for these disorders. Autoimmune disorders are characterised by mitochondrial dysfunction, oxidative stress, and inflammation; there is therefore a rationale for a role for coenzyme Q10 in the management of these disorders, on the basis of its key role in normal mitochondrial function, as an antioxidant, and as an anti-inflammatory agent. In this article, we have therefore reviewed the potential role of CoQ10, in terms of both deficiency and/or supplementation, in a range of autoimmune disorders. Full article
(This article belongs to the Special Issue Mitochondrial Dysfunction in Autoimmune Diseases)
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