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World J Respirol. Nov 28, 2013; 3(3): 77-103
Published online Nov 28, 2013. doi: 10.5320/wjr.v3.i3.77
Published online Nov 28, 2013. doi: 10.5320/wjr.v3.i3.77
Autotaxin and lysophosphatidic acid signalling in lung pathophysiology
Christiana Magkrioti, Vassilis Aidinis, Institute of Immunology, Biomedical Sciences Research Center Alexander Fleming, 16672 Athens, Greece
Author contributions: Magkrioti C and Aidinis V searched the literature, analyzed their results, wrote and revised the manuscript.
Supported by National Grants from the Hellenic Ministry of Education, Lifelong Learning and Religious Affairs, No. 09SYN-12-679/680
Correspondence to: Dr. Vassilis Aidinis, PhD, Researcher A’, Institute of Immunology, Biomedical Sciences Research Center Alexander Fleming, 34 Fleming Street, 16672 Athens, Greece. v.aidinis@fleming.gr
Telephone: +30-210-9654382 Fax: +30-210-9654210
Received: August 29, 2013
Revised: October 3, 2013
Accepted: November 18, 2013
Published online: November 28, 2013
Revised: October 3, 2013
Accepted: November 18, 2013
Published online: November 28, 2013
Core Tip
Core tip: In the lungs, autotaxin (ATX) is constitutively expressed in the bronchial epithelium, and all pulmonary cell types express some amount of lysophosphatidic acid (LPA) receptor. LPA affects all pulmonary cell types, mainly promoting a pro-inflammatory state. Increased ATX/LPA levels have been detected in various pathophysiological situations, both in mice and humans, including acute, allergic or chronic pulmonary inflammation; fibrosis; and lung cancer. Genetic or pharmacologic interventions targeting the ATX/LPA axis have proved beneficial for modelled disease management in animal models, establishing the ATX/LPA axis as a possible therapeutic target.