Toll-like receptor 2, hyaluronan, and neutrophils play a key role in plaque erosion: the OPTICO-ACS study.
Denitsa MetevaRamona VinciClaudio SeppeltYoussef S AbdelwahedDaniela PedicinoGregor NellesCarsten SkurkArash HaghikiaUrsula Rauch-KröhnertTeresa GerhardtElisabeth StraesslerYingjie ZhaoFelix GollaMichael JonerHimanshu RaiAdelheid KratzerHector Giral ArnalGiovanna LiuzzoJens KlotscheFilippo CreaUlf LandmesserDavid M LeistnerNicolle KränkelPublished in: European heart journal (2023)
The current study provides first in-human evidence for distinct TLR2-mediated neutrophil activation in IFC-ACS, presumably triggered by elevated soluble hyaluronic acid. Together with disturbed flow conditions, neutrophil-released MMP9 might be promoting endothelial cell loss-triggered thrombosis and therefore providing a potential future target for a phenotype-specific secondary therapeutic approach in IFC-ACS.