Atherosclerosis is a complex disease process in which genetic,
lipid, cellular, and
immunological factors combine to determine the location, severity, and timing of lesion development and clinical events. It has been demonstrated, however, that
inflammation governed
atherosclerosis during the course of development of
atherosclerosis. It has also been demonstrated to be effective to decrease the cardiovascular events and improve the prognosis of atherosclerotic diseases by regulating inflammatory reaction (e.g.,
statins). However, endogenous mechanisms of limiting
inflammation in
atherosclerosis are still unclear. Recent studies showed that
lipoxidase/
leukotrienes (LOX/LTs) pathway played important role in the ignition and development of
atherosclerosis, whereas resolvins (E-series resolvins and D-series resolvins) and protectins [
protectin D1 (PD1) and
neuroprotectin D1 (NPD1)], endogenous
lipid-derived mediators, inhibited
inflammation through pro-resolution and counter-modulating immune
inflammation reaction in
atherosclerosis. Hence, we hypothesize that increased endogenous
lipid mediators mentioned above play a vital role in anti-
atherosclerosis and plaque stabilization through pro-resolution and anti-
inflammation by LOX/LTs pathway. In addition, we predict that the endogenous
lipid mediators may be a new target for treatment of atherosclerotic diseases.