Abstract
Background. Transforming growth factor-β (TGF-β) plays a key role in the development and progression of diabetic nephropathy (DN), but the specific mechanisms of its influence on a number of processes underlying its development remain poorly understood. Aim: to analyze the literature and summarize the existing data on the specific mechanisms of action and the role of the TGF-β signaling pathway in the pathogenesis of DN. Materials and methods. Systematic analytical search of English-language publications in PubMed, ScienceDirect, Scopus and Web of Science Core Collection electronic databases. Results. TGF-β plays an important but complex role in the pathogenesis of DN. It is clearly involved in the progression of DN, although its precise contribution continues to be the subject of ongoing debate and research. Although TGF-β is essential for normal tissue repair and homeostasis, its expression in the diabetic environment contributes to the excessive accumulation of extracellular matrix, podocyte and tubular damage that are characteristic of DN. The mechanisms by which TGF-β turns from a potentially protective factor to a pathogenic one remain poorly understood. The close interaction between TGF-β, its signaling pathways (both canonical Smad and non-canonical), and other critical factors such as hyperglycemia, oxidative stress, inflammation, and the renin-angiotensin system adds to the complexity of the problem. Conclusion. The review of the literature emphasizes the important role of TGF-β in the development of DN, which justifies the need to develop and study the effect of new highly specific inhibitors of TGF-β signaling on preventing or slowing the progression of DN