Abstract
Immunoglobin A Nephropathy (IgAN) is the most common primary glomerulonephritis worldwide. Its development is characterized by the deposition of immune complexes that consist of abnormally galactozylated IgA1 molecules and IgG or IgA autoantibodies in the mesangium and the subsequent induction of renal injury. Recent research has shed light to many aspects of the pathogenesis of the disease, including the contribution of epigenetic modifications in its onset and progression. This review aims to present some of the most important epigenetic mechanisms mediating IgA1 development, including alterations in DNA methylation and histone modifications. Though a lot of progress has been made in this field, there is still a long way towards the full understanding of the epigenetics’ involvement in IgAN, which can finally lead to a new, more promising approach of IgAN patients.
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