Oh, what a surprise, blood vessels don’t like being smothered in fats. Who would’ve thought that ApoB lipoproteins, those little blobs of joy, could be party poopers and cause atherosclerosis? But wait, there’s more! Apparently, the bouncers of the lipid world, known as lipolysis, are supposed to keep things in check, especially in those skinny capillaries. But when it comes to the big boys, the large blood vessels, we were in the dark about how they handle the fatty gatecrashers.

Enter the hero of our story, the enzyme adipose triglyceride lipase (ATGL). It turns out, when you give ATGL the boot from the endothelium, the inner lining of our vessels starts hoarding neutral lipids like they’re going out of style. This, of course, leads to the vessels throwing a fit, messing up their tone and their ability to produce nitric oxide, which is basically their chill pill.

And how does ATGL’s absence throw such a wrench in the works? It kicks off a drama in the endoplasmic reticulum, causing it to stress out and inflame the endothelium. It’s like a bad soap opera that ends with bigger and badder atherosclerotic lesions when you knock out endothelial ATGL. So, in a plot twist that shocks no one, the way fatty acids play musical chairs with lipid droplets is a big deal for keeping endothelial cells happy and vessels functioning properly, both on a sunny day and in the gloomy world of chronic disease.

But hey, at least now we know, right? Managing fat in large vessels is as crucial as a bouncer at a nightclub. Who knew science could be so… greasy?