Abstract
Renal fibrosis is final common pathway of end stage renal disease. Irrespective of the primary cause, renal fibrogenesis is a dynamic process which involves a large network of cellular and molecular interaction, including pro-inflammatory cell infiltration and activation, matrix-producing cell accumulation and activation, and secretion of profibrogenic factors that modulate extracellular matrix (ECM) formation and cell-cell interaction. Bone morphogenetic protein-7 is a protein of the TGF-β super family and increasingly regarded as a counteracting molecule against TGF-β. A large variety of evidence shows an anti-fibrotic role of BMP-7 in chronic kidney disease, and this effect is largely mediated via counterbalancing the profibrotic effect of TGF-β. Besides, BMP-7 reduced ECM formation by inactivating matrix-producing cells and promoting mesenchymal-to-epithelial transition (MET). BMP-7 also increased ECM degradation. Despite these observations, the anti-fibrotic effect of BMP-7 is still controversial such that fine regulation of BMP-7 expression in vivo might be a great challenge for its ultimate clinical application.
Highlights
Renal fibrosis, which characterized as glomerulosclerosis and tubulointerstitial fibrosis, is considered the hallmark of progressive renal injury and the final common pathway of multiple chronic renal diseases
This review focuses on role of BMP-7 in fibrotic kidney disease, and the possible mechanisms involved
Based on the overall results from all in vitro and in vivo studies to date, the anti-fibrotic effect of BMP-7 seems promising, whereas the diverse regulatory effect of BMP-7 in extracellular matrix (ECM) protein and gene expression, and its interaction with profibrotic mediators like connective tissue growth factor (CTGF) indicates that the precise role of BMP-7 could shift between anti-fibrosis or profibrosis and the fine regulation of its level in vivo might be a major challenge in the systemic use of BMP-7 in clinical application
Summary
Renal fibrosis, which characterized as glomerulosclerosis and tubulointerstitial fibrosis, is considered the hallmark of progressive renal injury and the final common pathway of multiple chronic renal diseases. TGF-β has been known as the key modulator of kidney (and that of other organs) fibrosis, and the role of TGF-β in renal fibrosis has been extensively studied. In recent years, another protein, BMP-7, that belongs to the TGF-β superfamily, has drawn great attention for its function in counteracting pro-fibrotic effects of TGF-β. BMP-7 is a homodimeric protein that with cysteine-knot It plays an crucial role in renal development and only selectively expressed in several adult organs including the kidney. This review focuses on role of BMP-7 in fibrotic kidney disease, and the possible mechanisms involved
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