This is correct. Dietary saturated fat is more of an issue for some vs dietary cholesterol. As you correctly pointed out, LDL synthesis and reuptake happens in the liver in response to various conditions in the body.
The actual reason plaques accumulate is well understood by the scientific community. It's less well understoood and communicated by cardiologists and the medical community in general. At the level of the lay person there are all kinds of wacky theories.
In short, endothelial damage occurs from any number of various reasons like hypertension, metabolic syndrome, chronic inflammation, or oxidative stress. Once damaged, atherogenic particles enter the subendothelial space and from there the process begins. I'll spare you the details of the process.
There are two primary aspects to this that are individually necessary, but not sufficient to cause ASCVD which requires both. That is to say, there must be endothelial damage and there must be atherogenic particles. There are people with elevated biomarkers for atherogenic particles that are otherwise genetically gifted with regard to the endothelial resilience that do not suffer from ASCVD. There are people that lost the genetic lottery in that sense or suffer from any number of conditions that exacerbate endothelial damage (like smoking) that a small number of atherogenic particles is sufficient to cause a great deal of disease.
This is why outcome trials are necessary for any particular intervention. Niacin, for example, improves biomarkers, but negatively impact outcomes. Generally speaking, outcome trials are the final step in drug development.
Most recently, the drug bempedoic acid show positive outcomes in the CLEAR outcomes trial which was completed in late 2023. Prior to that, Repatha (evolocumab) demonstrated positive outcomes in the FOURIER trial.
