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l‐α‐Lysophosphatidylinositol (LPI) aggravates myocardial ischemia/reperfusion injury via a GPR55/ROCK‐dependent pathway
Raised levels of LPI in the vicinity of a developing infarct may worsen the outcome of AMI, and activation of the Rho kinase/ROCK/p38 MAPK pathway is responsible for LPI‐induced extension of I/R injury.
Studies on the role of GPR55 in cardiovascular physiology and pathophysiology
Evidence is provided that GPR 55 may have the potential to be targeted for therapeutic gains in atherosclerosis and myocardial I/R injury and the signalling mechanisms by which GPR55 elicits any observed effects on the myocardium in response to such injury.