TY - JOUR
T1 - Inflammation and renal fibrosis
T2 - Recent developments on key signaling molecules as potential therapeutic targets
AU - Lv, Wenshan
AU - Booz, George W.
AU - Wang, Yangang
AU - Fan, Fan
AU - Roman, Richard J.
N1 - Publisher Copyright:
© 2017 Elsevier B.V.
PY - 2018/2/5
Y1 - 2018/2/5
N2 - Chronic kidney disease (CKD) is a major public health issue. At the histological level, renal fibrosis is the final common pathway of progressive kidney disease irrespective of the initial injury. Considerable evidence now indicates that renal inflammation plays a central role in the initiation and progression of CKD. Some of the inflammatory signaling molecules involved in CKD include: monocyte chemoattractant protein-1 (MCP-1), bradykinin B1 receptor (B1R), nuclear factor κB (NF-κB), tumor necrosis factor-α (TNFα), transforming growth factor β (TGF-β), and platelet-derived growth factor (PDGF). Multiple antifibrotic factors, such as interleukin-10 (IL-10), interferon-γ (IFN-γ), bone morphogenetic protein-7 (BMP-7), hepatocyte growth factor (HGF) are also downregulated in CKD. Therefore, restoration of the proper balance between pro- and antifibrotic signaling pathways could serve as a guiding principle for the design of new antifibrotic strategies that simultaneously target many pathways. The purpose of this review is to summarize the existing body of knowledge regarding activation of cytokine pathways and infiltration of inflammatory cells as a starting point for developing novel antifibrotic therapies to prevent progression of CKD.
AB - Chronic kidney disease (CKD) is a major public health issue. At the histological level, renal fibrosis is the final common pathway of progressive kidney disease irrespective of the initial injury. Considerable evidence now indicates that renal inflammation plays a central role in the initiation and progression of CKD. Some of the inflammatory signaling molecules involved in CKD include: monocyte chemoattractant protein-1 (MCP-1), bradykinin B1 receptor (B1R), nuclear factor κB (NF-κB), tumor necrosis factor-α (TNFα), transforming growth factor β (TGF-β), and platelet-derived growth factor (PDGF). Multiple antifibrotic factors, such as interleukin-10 (IL-10), interferon-γ (IFN-γ), bone morphogenetic protein-7 (BMP-7), hepatocyte growth factor (HGF) are also downregulated in CKD. Therefore, restoration of the proper balance between pro- and antifibrotic signaling pathways could serve as a guiding principle for the design of new antifibrotic strategies that simultaneously target many pathways. The purpose of this review is to summarize the existing body of knowledge regarding activation of cytokine pathways and infiltration of inflammatory cells as a starting point for developing novel antifibrotic therapies to prevent progression of CKD.
KW - Antifibrotic therapy
KW - Chronic kidney disease
KW - Cytokines
KW - Inflammation
KW - Renal fibrosis
UR - http://www.scopus.com/inward/record.url?scp=85038103081&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85038103081&partnerID=8YFLogxK
U2 - 10.1016/j.ejphar.2017.12.016
DO - 10.1016/j.ejphar.2017.12.016
M3 - Review article
C2 - 29229532
AN - SCOPUS:85038103081
SN - 0014-2999
VL - 820
SP - 65
EP - 76
JO - European Journal of Pharmacology
JF - European Journal of Pharmacology
ER -