https://scholars.lib.ntu.edu.tw/handle/123456789/531837
標題: | Lysophosphatidic acid and renal fibrosis | 作者: | JENQ-WEN HUANG HUI-TENG CHENG CHIH-KANG CHIANG KUAN-YU HUNG TUN-JUN TSAI |
公開日期: | 2008 | 卷: | 2 | 期: | 3 | 起(迄)頁: | 204-210 | 來源出版物: | Recent Patents on Endocrine, Metabolic and Immune Drug Discovery | 摘要: | Lysophosphatidic acid (LPA) and its specific G-protein-coupled receptors have mitogen-like activities in cellular signal transduction. At the intracellular level, LPA is produced by phospholipase A1 (PLA1) or PLA2; at the extracellular level, LPA is produced by autotaxin/ lysophospholipase D. Lipid phosphate phosphatases (LPPs) dephosphorylate LPA and thereby attenuate LPA signaling. Chronic kidney diseases (CKDs) and end-stage renal disease (ESRD) are significant public health issues throughout the world. In these conditions, there is a production and accumulation of transforming growth factor (TGF-β) and connective tissue growth factor (CTGF), leading to accumulation of extracellular matrix proteins and renal fibrosis. In addition, CKD risk factors such as diabetes mellitus, hypertension, dyslipidemia, and activation of the renin-angiotensin- aldosterone system can lead to overexpression of the TGF-β-CTGF-collagen/fibronectin axis and thereby accelerate formation of renal fibrosis. More than five LPA receptors (LPA1 - LPA5) have been identified and have been shown to be expressed in different tissues. LPA1 mediates lung and renal fibrosis following injury, and Ki16425 has been shown to be an antagonist of the LPA1 receptor and an attenuator of fibrosis formation. In this review, we provide a brief update on the concepts of renal fibrosis and the pathogenetic roles of the different LPA signaling pathways, discuss some recent patents on pharmaceuticals that disrupt these pathways, and introduce some pilot studies that have explored the therapeutic potentials of LPA receptor antagonists for management of renal fibrosis. ? 2008 Bentham Science Publishers Ltd. |
URI: | https://www.scopus.com/inward/record.uri?eid=2-s2.0-58149131354&doi=10.2174%2f187221408786241856&partnerID=40&md5=298c1796f7384f0b5da336cc3c51a1b7 https://scholars.lib.ntu.edu.tw/handle/123456789/531837 |
ISSN: | 1872-2148 | DOI: | 10.2174/187221408786241856 | SDG/關鍵字: | 2,4 thiazolidinedione derivative; 3 [4[4[[1 (2 chlorophenyl)ethoxy]]carbonylamino] 3 methyl 5 isoxazolyl]benzylsulfanylpropanoic acid; autotaxin; collagen; connective tissue growth factor; fibronectin; G protein coupled receptor; ki 16425; lysophosphatidic acid; lysophosphatidic acid receptor; lysophosphatidic acid receptor 1; lysophosphatidic acid receptor 2; lysophosphatidic acid receptor 3; lysophosphatidic acid receptor 4; lysophosphatidic acid receptor 5; lysophosphatidic acid receptor agonist; lysophosphatidic acid receptor antagonist; lysophospholipase; lysophospholipase D; peroxisome proliferator activated receptor gamma agonist; phosphatidate phosphatase; phospholipase A1; phospholipase A2; scleroprotein; transforming growth factor; unclassified drug; urinary tract agent; chronic kidney disease; diabetes mellitus; disease course; disease model; drug mechanism; dyslipidemia; human; hypertension; in vivo study; kidney failure; kidney fibrosis; nonhuman; patent; pathogenesis; priority journal; protein analysis; protein dephosphorylation; protein expression; protein function; public health; receptor intrinsic activity; renin angiotensin aldosterone system; review; risk factor; signal transduction |
顯示於: | 醫學系 |
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