Molecular and cellular mechanisms and mediator system of kidney and heart remodeling in chronic kidney disease — the target of nephro-and cardioprotection

И. Н. Бобкова¹, Л. В. Козловская¹, М. Л. Нанчикеева², Н. В. Чеботарёва¹, О. А. Ли¹

Authors: N. Bobkova1, L. V. Kozlovskaya1, M. L. Nanchikeeva2, N. V. Chebotareva1, A. O. Li1

Place: Moscow, Russia
Vladimir, Russia

Institution: 1 First Moscow State Medical University named after I. M. Sechenov, Moscow, Russia 2 Regional Hospital, Vladimir, Russia

Abstract: The lecture reviews molecular and cellular mechanisms, which are cornerstone of structural and functional remodeling and kidney and heart fibrosis formation in chronic kidney disease. The key ways linking kidney and heart remodeling, including myofibroblast formation by epithelial-mesenchymal and endotelial-mesenchymal transdifferentiation, extracellular matrix production, are presented. The role of angiotensin II, transforming growth factor B1, plasminogen activator inhibitor type I, vascular endothelial growth factor, matrix metalloproteinases and tissue inhibitors of matrix metalloproteinases in mechanisms of fibro- and angiofibrogenesis are discussed. Further research of the molecular and cellular mechanisms of tissue fibrosis broadens our understanding about nephro- and cardioprotective effects of traditional approaches (angiotensin converting enzyme inhibitors or angiotensin II receptor blockers) and gives an opportunity for therapy targeting common mediators of fibro- and angiofibrogenesis in kidneys and heart.  

Keywords: renal and cardiac remodeling, epithelial-mesenchymal transdifferentiation, endothelial-mesenchymal transdifferentiation, myofibroblasts, angiotensin II, mediators of fibrosis, cardio-nephroprotection

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