期刊
BRITISH JOURNAL OF PHARMACOLOGY
卷 161, 期 2, 页码 241-270出版社
WILEY
DOI: 10.1111/j.1476-5381.2010.00815.x
关键词
lysophospholipid; cyclic phosphatidic acid; alkyl glycerophosphate; endothelial differentiation gene; GPR23; GPR92; GPR87; P2Y5; P2Y10; PPAR gamma
资金
- NIH [CA92160, HL79004, AI080405]
- NATIONAL CANCER INSTITUTE [R01CA092160] Funding Source: NIH RePORTER
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL079004] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI080405] Funding Source: NIH RePORTER
Lysophosphatidic acid (LPA, 1-radyl-2-hydroxy-sn-glycero-3-phosphate) is the prototype member of a family of lipid mediators and second messengers. LPA and its naturally occurring analogues interact with G protein-coupled receptors on the cell surface and a nuclear hormone receptor within the cell. In addition, there are several enzymes that utilize LPA as a substrate or generate it as a product and are under its regulatory control. LPA is present in biological fluids, and attempts have been made to link changes in its concentration and molecular composition to specific disease conditions. Through their many targets, members of the LPA family regulate cell survival, apoptosis, motility, shape, differentiation, gene transcription, malignant transformation and more. The present review depicts arbitrary aspects of the physiological and pathophysiological actions of LPA and attempts to link them with select targets. Many of us are now convinced that therapies targeting LPA biosynthesis and signalling are feasible for the treatment of devastating human diseases such as cancer, fibrosis and degenerative conditions. However, successful targeting of the pathways associated with this pleiotropic lipid will depend on the future development of as yet undeveloped pharmacons.
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