https://www.atherosclerosis-journal.com/article/S0021-9150(18)31457-6/fulltext

Nice publication. A poster version of this manuscript was recently presented at the ASN conference (see here). A lot of this is beyond my expertise and is in detail beyond what most on this board care about. But I copied, pasted and paraphrased to create a summary paragraph below (same summary as my previous post). Also, I previously addressed some of Tada's questions on this paper when it first came out last week. 

Vascular calcification (VC) leads to pathological vascular stiffness, is prevalent in chronic kidney disease (CKD), and increases cardiovascular risk (increased MACE incidence). VC occurs in a region of the vessel wall comprised of vascular smooth muscle cells (VSMCs). During VC, VSMCs transdifferentiate into osteoblast-like cells that promote calcification. Previous proteomic analysis of patient blood samples treated with apabetalone showed reduced circulating proteins & pathways associated with VC. This current study directly looked at apabetalone's effects on primary human coronary artery VSMCs. Long story short, apabetalone reduced expression of markers of VSMC transdifferentiation into osteoblast-like cells and reduced expression of genes that promote calcification of VSMCs. This data demonstrate for the first time that VSMC calcification is mediated by BET proteins and is sensitive to BETi. One BET protein, BRD4, has been previously linked to calcification. They used some state of the art techniques (i.e. chromatin immunoprecipitation w/ DNA sequencing; aka ChIP-Seq) to show that BRD4 distribution on the DNA changes during transdifferentiation of the VSMC into the osteoblast-like cells, particularly in "enhancer" regions associated wiht high levels of gene expression. Apabetalone reduced the number, length and area of these BRD4-rich enhancers, consistent with displacement of BRD4 from chromatin.