A team of Japanese researchers found that LDL may contribute to vascular diseases by a previously unidentified mechanism involving the activation of vascular endothelial growth factor receptor 1 (VEGFR1).
Using cell lines and mouse models, the investigators discovered that when native LDL (nLDL) is bound to the LDL receptor, it can activate VEGFR1 and accelerate migration of macrophages, which accumulate in the plaques. Both these effects could contribute to the progression of plaques and blocking of arteries, report the authors.
The research was conducted by scientists at Tokyo Women’s Medical University, the University of Tokyo, and Jichi Medical University. The study is published online October 26 in EMBO reports.