This review demonstrates the role of non-coding RNAs in myofibroblast differentiation from monocytes, suggesting they may drive fibrosis through epigenetic mechanisms.
Recently, more and more attention has been paid to the study of the role of epigenetic mechanisms in the development and progression of immunoinflammatory diseases accompanied by the development of fibrosis. Epigenetic modifications, compared with genetic changes that persist throughout the life of an organism, are extremely dynamic and can differ both in different cell populations and in the same cell depending on the stage of differentiation and microenvironment. The review summarizes information on the potential role of key epigenetic factors, in particular non-coding RNAs, in the differentiation of circulating bone marrow-derived monocytes into myofibroblasts, cellular mediators of fibrosis. Due to their high plasticity and ability to phenotypic transformation, monocytes and macrophages are the most important participants in tissue homeostasis and play a key role in the development of fibrosis at all stages of tissue repair, from inflammation to remodeling.
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O.V. Balan (2025) studied this question.
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