期刊
FRONTIERS IN PHYSIOLOGY
卷 6, 期 -, 页码 -出版社
FRONTIERS MEDIA SA
DOI: 10.3389/fphys.2015.00114
关键词
BMP-7; chronic kidney disease; renal fibrosis; cytokines; inflammation
类别
资金
- General Research Fund of the Research Grants Council of Hong Kong [HKU7770/09M]
- National Basic Research Program of China 973 program [2012CB517600, 2012CB517606]
- Hong Kong Concrete and the Continental Cement and Gypsum Co. Ltd.
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-beta super family and increasingly regarded as a counteracting molecule against TGF-beta. 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-beta. Besides, BMP-7 reduced ECM formation by inactivating matrix-producing cells and promoting mesenchymal-to-epithelial transition (MET). BM P-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.
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