Abstract
Systemic lupus erythematosus (SLE) is a potentially fatal multisystem inflammatory chronic disorder, the etiology and pathogenesis of which remain unclear. The loss of immune tolerance in SLE patients contributes to the production of autoantibodies that attack multiple organs and tissues, such as the skin, joints, and kidneys. Immune cells play important roles in the occurrence and progression of SLE through amplified immune responses. Sirtuin-1 (SIRT1), an NAD+-dependent histone deacetylase, has been shown to be a pivotal regulator in various physiological processes, including cell differentiation, apoptosis, metabolism, aging, and immune responses, via modulation of different signaling pathways, such as the nuclear factor κ-light-chain-enhancer of activated B cells and activator protein 1 pathways. Recent studies have provided evidence that SIRT1 could be a regulatory element in the immune system, whose altered functions are likely relevant to SLE development. This review aims to illustrate the functions of SIRT1 in different types of immune cells and the potential roles of SIRT1 in the SLE pathogenesis and its therapeutic perspectives.
Highlights
Systemic lupus erythematosus (SLE), a typical prototype of connective tissue diseases, is characterized by immunocomplex-mediated inflammation
The complexity of SLE is indicated by involvement of multiple organs and various clinical features, such as arthritis, nephritis, vasculitis, and pleuritis or pericarditis, and abnormal laboratory examinations, such as decreased complements and increased levels of autoantibodies including antinuclear antibodies (ANAs), anti-Smith (Sm) antibodies, and anti-double-stranded DNA antibodies [1]
Epigenetic mechanisms in SLE mainly include DNA methylation, histone modification, and non-coding RNA modification, among which DNA hypomethylation was the first epigenetic pattern determined in SLE patients [4]
Summary
Systemic lupus erythematosus (SLE), a typical prototype of connective tissue diseases, is characterized by immunocomplex-mediated inflammation. The complexity of SLE is indicated by involvement of multiple organs and various clinical features, such as arthritis, nephritis, vasculitis, and pleuritis or pericarditis, and abnormal laboratory examinations, such as decreased complements and increased levels of autoantibodies including antinuclear antibodies (ANAs), anti-Smith (Sm) antibodies, and anti-double-stranded DNA (dsDNA) antibodies [1]. The pathogenesis of SLE has been explored from the level of histopathology to molecular biology, the pathogenic mechanisms underlying this disease remain unclear. Epigenetic modifications can be described as modulation of gene expression without changing the original sequence of the genetic code or inheritable and reversible alterations during transcription activity [3]. Epigenetic mechanisms in SLE mainly include DNA methylation, histone modification, and non-coding RNA modification, among which DNA hypomethylation was the first epigenetic pattern determined in SLE patients [4]
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