Dynamic changes of the composition of plasmaHDLparticles in patients with cardiac disease: Spotlight on sphingosine‐1‐phosphate/serum amyloid A ratio

Abstract

SummarySeveral epidemiological studies reported an inverse relationship between plasma highdensity lipoprotein (HDL) cholesterol levels and atherosclerotic cardiovascular disease (ASCVD). However, therapeutic interventions targeted at raising HDL-cholesterol failed to improve cardiovascular outcomes, suggesting that HDL components distinct from cholesterol may account for the anti-atherothrombotic effects attributed to this lipoprotein. Sphingosine-1-phosphate (S1P) and the acute phase protein serum amyloid A (SAA) have been identified as integral constituents of HDL particles. Evidence suggests that S1P and SAA levels within HDL particles may be affected by inflammation and oxidative stress, which are coexisting processes underlying ASCVD. Because SAA, an inflammation-related marker, and S1P, an anti-atherothrombotic marker, have relatively clear opposite characteristics among the HDL-associated proteins, the approach of assessing the two markers simultaneously may provide new insights in clinical practice (S1P/SAA Index). This review focuses on evidence in support of the concept that the S1P/SAA Index may affect the HDL atheroprotective properties and may, therefore represent a potential target for therapeutic interventions. K E Y W O R D Satherosclerotic cardiovascular disease, high-density lipoprotein, serum amyloid A, sphingosine- , showed that low HDL-cholesterol levels are an independent risk factor for ASCVD and estimated that an increase of 1 mg/dL (0.026 mmol/L) in HDLcholesterol is associated with a 2%-3% of risk reduction. 8,9 Further

The Lipid Status in Patients with Ulcerative Colitis: Sphingolipids are Disease-Dependent Regulated

“…These data indicate that the plasma S1P level can be up- or down-regulated under various inflammatory conditions and that further studies investigating where plasma S1P comes from are needed. Erythrocytes are one of the main S1P sources, but also binding of S1P to high-density lipoprotein or serum albumin might be an important mechanism that contributes to alterations in the serum S1P level [49]. However, even we and others could not detect a disease-dependent change in the plasma S1P level; manipulation of the S1P signaling pathway by treating UC patients with ozanimod seems to be a promising approach that several clinical trials are ongoing, investigating S1P modulators in IBD [50].…”