PMID- 29229532 OWN - NLM STAT- MEDLINE DCOM- 20180806 LR - 20201123 IS - 1879-0712 (Electronic) IS - 0014-2999 (Print) IS - 0014-2999 (Linking) VI - 820 DP - 2018 Feb 5 TI - Inflammation and renal fibrosis: Recent developments on key signaling molecules as potential therapeutic targets. PG - 65-76 LID - S0014-2999(17)30800-2 [pii] LID - 10.1016/j.ejphar.2017.12.016 [doi] 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 B(1) receptor (B(1)R), nuclear factor kappaB (NF-kappaB), tumor necrosis factor-alpha (TNFalpha), transforming growth factor beta (TGF-beta), and platelet-derived growth factor (PDGF). Multiple antifibrotic factors, such as interleukin-10 (IL-10), interferon-gamma (IFN-gamma), 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. CI - Copyright (c) 2017 Elsevier B.V. All rights reserved. FAU - Lv, Wenshan AU - Lv W AD - Department of Pharmacology and Toxicology, University of Mississippi Medical Center, Jackson, MS 39216, USA; Department of Endocrinology and Metabolism, the Affiliated Hospital of Qingdao University, Qingdao 26003, China. FAU - Booz, George W AU - Booz GW AD - Department of Pharmacology and Toxicology, University of Mississippi Medical Center, Jackson, MS 39216, USA. FAU - Wang, Yangang AU - Wang Y AD - Department of Endocrinology and Metabolism, the Affiliated Hospital of Qingdao University, Qingdao 26003, China. FAU - Fan, Fan AU - Fan F AD - Department of Pharmacology and Toxicology, University of Mississippi Medical Center, Jackson, MS 39216, USA. FAU - Roman, Richard J AU - Roman RJ AD - Department of Pharmacology and Toxicology, University of Mississippi Medical Center, Jackson, MS 39216, USA. Electronic address: rroman@umc.edu. LA - eng GR - R01 DK104184/DK/NIDDK NIH HHS/United States GR - R01 AG057842/AG/NIA NIH HHS/United States GR - R21 AG050049/AG/NIA NIH HHS/United States GR - P20 GM104357/GM/NIGMS NIH HHS/United States GR - R01 HL138685/HL/NHLBI NIH HHS/United States GR - R37 HL036279/HL/NHLBI NIH HHS/United States GR - R01 HL036279/HL/NHLBI NIH HHS/United States PT - Journal Article PT - Review DEP - 20171208 PL - Netherlands TA - Eur J Pharmacol JT - European journal of pharmacology JID - 1254354 SB - IM MH - Animals MH - Fibrosis MH - Humans MH - Inflammation/drug therapy/pathology MH - Kidney/*drug effects/*pathology MH - Molecular Targeted Therapy/*methods MH - Signal Transduction/drug effects PMC - PMC6733417 MID - NIHMS928988 OTO - NOTNLM OT - Antifibrotic therapy OT - Chronic kidney disease OT - Cytokines OT - Inflammation OT - Renal fibrosis EDAT- 2017/12/13 06:00 MHDA- 2018/08/07 06:00 PMCR- 2019/09/09 CRDT- 2017/12/13 06:00 PHST- 2017/09/29 00:00 [received] PHST- 2017/12/07 00:00 [revised] PHST- 2017/12/07 00:00 [accepted] PHST- 2017/12/13 06:00 [pubmed] PHST- 2018/08/07 06:00 [medline] PHST- 2017/12/13 06:00 [entrez] PHST- 2019/09/09 00:00 [pmc-release] AID - S0014-2999(17)30800-2 [pii] AID - 10.1016/j.ejphar.2017.12.016 [doi] PST - ppublish SO - Eur J Pharmacol. 2018 Feb 5;820:65-76. doi: 10.1016/j.ejphar.2017.12.016. Epub 2017 Dec 8.