Epigenetic linkage of systemic lupus erythematosus and nutrition

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Abstract

The term 'epigenetics' refers to a series of meiotically/mitotically inheritable alterations in gene expression, related to environmental factors, without disruption on DNA sequences of bases. Recently, the pathophysiology of autoimmune diseases (ADs) has been closely linked to epigenetic modifications. In fact, epigenetic mechanisms can modulate gene expression or repression of targeted cells and tissues involved in autoimmune/inflammatory conditions acting as keys effectors in regulation of adaptive and innate responses. ADs, as systemic lupus erythematosus (SLE), a rare disease that still lacks effective treatment, is characterised by epigenetic marks in affected cells. Taking into account that epigenetic mechanisms have been proposed as a winning strategy in the search of new, more specific and personalised therapeutics agents, pharmacology and pharmaco-epigenetic studies about epigenetic regulations of ADs may provide novel individualised therapies. Focusing on possible implicated factors on development and predisposition of SLE, diet is feasibly one of the most important factors since it is linked directly to epigenetic alterations and these epigenetic changes may augment or diminish the risk of SLE. Nevertheless, several studies have suggested that dietary therapy could be promising to SLE patients via prophylactic actions deprived of side effects of pharmacology, decreasing co-morbidities and improving lifestyle of SLE sufferers. Herein, we review and discuss the cross-link between epigenetic mechanisms on SLE predisposition and development, as well as the influence of dietary factors on regulation of epigenetic modifications that may eventually make a positive impact on SLE patients.

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Montoya, T., Castejón, M. L., Muñoz-García, R., & Alarcón-De-La-Lastra, C. (2023, June 16). Epigenetic linkage of systemic lupus erythematosus and nutrition. Nutrition Research Reviews. Cambridge University Press. https://doi.org/10.1017/S0954422421000287

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