Interesting study comparing BAM15 to atorvastatin.
"In summary, the in vivo experiments demonstrated that oral administration of BAM15 significantly reduced the increased plaque area and the increased necrotic core area of plaque induced by WD feeding in ApoE(−/−) mice. In in vitro experiments, cell biological assays confirmed that BAM15 inhibited RAW264.7 macrophages invasive ability and reduced PA-induced lipid accumulation. By combining RNA-seq techniques, molecular docking, and experimental validation, we found that IL-1α, SRC, and CSF3 are key anti-AS molecules of BAM15.
This study reveals that BAM15 may be a promising drug against AS, providing scientific evidence to reveal the pharmacological mechanism of BAM15 in the treatment of AS, and facilitating future clinical translational research."
The practical question is what’s causing what. Clinical trials and mendelian randomization studies that separately investigate a change in either apoB or apoA-1 levels tells us whether it’s higher apoB or lower apoA-1 that’s increasing the risk, or vice versa lower apoB or higher apoA-1 that is decreasing the risk, if that makes sense.
So correct me if I’m wrong if you believe that the ratio is a better predictor than apoB you would need to know whether apoA-1 independently changes risk of apoB levels, as that would tell you whether a lower ratio from higher apoA-1 levels would decrease risk.
Atherosclerotic blood vessel cells grow similar to tumors, study reveals
"Researchers from the University of Southern Denmark and Odense University Hospital have studied tissue from patients with atherosclerosis. They found that many of the cells in the diseased tissue carried the same genetic alteration and appeared to originate from a single ancestral cell that had divided repeatedly—a pattern otherwise associated with tumor biology.
In several patients, a large proportion of the cells were derived from one single mutated cell that had undergone many rounds of cell division.
“It’s striking how many cells in the tissue share the exact same genetic change. In several samples, more than 10% of the cells—hundreds of thousands cells—carried the same alteration. It’s difficult to interpret this as anything other than all these cells originating from a shared ancestral cell that, at some point during disease development, acquired the mutation,” says Lasse Bach Steffensen, Associate Professor at the Department of Molecular Medicine at the University of Southern Denmark.
In a tumor, the disease often begins when a single cell acquires a genetic alteration that causes it to divide more than it should. As the daughter cells inherit the same alteration and continue to divide, a progressively larger mass of cells forms—what we call a tumor.
This finding offers a new perspective on atherosclerosis—a disease primarily associated with cholesterol, inflammation and lifestyle factors."