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Autotaxin‐LPA‐LPP3 axis regulates mitochondrial respiration prompting myocardial dysfunction

Acute myocardial infarction (AMI) and ischemic heart disease are the two most prevalent causes of morbidity and mortality in the western world. Lysophosphatidic acid (LPA) a pro‐inflammatory, pro‐thrombotic bioactive glycerophospholipid plays a well‐known role in atherosclerotic disease; its role in myocardial dysfunction remains virtually unexplored. Following AMI, serum LPA concentration increases six‐fold over control subjects. Since LPA has a rapid turnover in the circulation, LPA production involves hydrolysis of lysophosphatidylcholine by the secreted enzyme autotaxin.