Targeting Bone Marrow-Derived Fibroblasts for Renal Fibrosis
Renal fibrosis is a major pathological feature of chronic kidney disease, which is characterized by massive fibroblast activation and excessive production and deposition of extracellular matrix (ECM). Renal fibrosis results in progressive loss of kidney function; however, there is currently no effective therapy available clinically to treat or even reverse renal fibrosis. Although activated fibroblasts/myofibroblasts are responsible for the production and deposition of ECM, their origin has been debatable. Recent studies have provided compelling evidence that bone marrow-derived fibroblast precursors contribute significantly to the population of myofibroblasts and the development of renal fibrosis. Therefore, targeting the molecular signaling mechanisms underlying the recruitment and activation of the bone marrow-derived fibroblast precursors may serve as novel therapeutic strategy for chronic kidney disease. In this review, we appraise recent advances in our understanding of the recruitment and activation of bone marrow-derived fibroblast precursors in the kidney and the development of renal fibrosis and highlight novel molecular signaling pathways that may lead to the development of new therapies for chronic kidney disease.
KeywordsChemokine Cytokine Bone marrow-derived fibroblast precursors Fibroblasts Renal fibrosis Extracellular matrix Chronic kidney disease Monocyte-to-fibroblast transition
This work was supported by grants from the National Institutes of Health grant (R01DK95835) and the US Department of Veterans Administration grant (I01BX02650) to YW. This chapter was modified from an article authored by our group in Frontiers in Physiology (Yan et al. 2016). The related contents are reused with permission.
Conflict of Interest Statement
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be considered as a potential conflict of interest.
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