Exploring the Pathogenesis and Treatment of IgA Nephropathy Based on Epigenetics

Abstract

IgA nephropathy is the most common primary glomerulonephritis worldwide. However, its exact cause remains unclear, with known genetic factors explaining only 11% of the variation. Recently, researchers have turned their attention to epigenetic abnormalities in immune-related diseases, recognizing their significance in IgA nephropathy’s development and progression. This emerging field has revolutionized our understanding of epigenetics in IgA nephropathy research. Though in its early stages, studying IgA nephropathy’s epigenetics holds promise for unraveling its pathogenesis and identifying new biomarkers and therapies. This review aims to comprehensively analyze epigenetics’ role in IgA nephropathy’s development and suggest avenues for potential therapeutic interventions. In the future, assessing and modulating epigenetics may become integral in diagnosing, tailoring treatments and assessing prognoses for IgA nephropathy.

Graphical abstract

Epigenetics is involved in the occurrence and development of IgA nephropathy.

Keywords::

• epigenetic
• histone modifications
• IgA nephropathy
• methylation
• miRNAs
• pathogenesis
• treatment

Financial disclosure

This work was supported in part by the National Natural Science Foundation of China (project no. 81300583), Science and Technology Innovation Project of Fujian Province (project no.2019Y9043), Key Project of Social Development of Fujian Province of China (project no.2019Y0069), Key Project of Social Development of Fujian Province of China (project no.2023Y0068) and Foundation of The 900th Hospital of Joint Logistic Team (project no.2021MS15, 2021JQ10, 2022MS30, 2022ZD05, 2023ON02). The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

Competing interests disclosure

The authors have no competing interests or relevant affiliations with any organization or entity with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

Writing disclosure

No writing assistance was utilized in the production of this manuscript.