Tiny particles called PM2. 5 can make atherosclerotic plaques in our arteries unstable, although scientists aren't sure exactly how they do this. To figure it out, scientists fed a high-fat diet and gave vitamin D3 injections to 56 Wistar rats to create atherosclerotic models. These rats were then divided into groups and exposed to different amounts of PM2. 5 for four weeks.

When they looked at the rats' aortas, they found that PM2. 5 made the collagen fibers thinner and the muscle fibers disorganized. It also affected the expression of certain genes like MMP2, MMP9, TIMP2, and vimentin, which are related to plaque stability.

PM2. 5 exposure also increased the activity of the Notch signaling pathway. This pathway is important because it's linked to how stable our artery plaques are. Additionally, PM2. 5 increased the rate of cell death in foam cells, which are involved in atherosclerosis.

In foam cells, higher doses of PM2. 5 led to more MMP2, MMP9, and vimentin, but less TIMP2. When the Notch signaling pathway was blocked, the changes in plaque stability-related genes were reduced. This suggests that the Notch signaling pathway plays a key role in how PM2. 5 affects atherosclerosis.

So, the bottom line is that PM2. 5 exposure can make our artery plaques unstable, making atherosclerosis worse. The Notch signaling pathway seems to be a crucial part of this process.

Tiny Particles, Big Problems: How PM2. 5 Affects Artery Plaques

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