Thread by @Marion436842126

1/6 Statins can Induce the Accumulation of Regulatory T Cells in Atherosclerotic Plaque. I’ve seen studies where Globally depleting all CD8+ T cells (Tregs) reduces atherosclerotic lesion formation, which uncovers a function of CD8+ T cells in monocyte production in the bone /2

2/6 marrow, subsequently controlling plaque macrophage accumulation. The other issue is that Statins promote apoptosis in vascular smooth muscle cells causing dysfunction and erosion of endothelial cell integrity, resulting in thrombus formation and myocardial infarction /3

3/6 One study suggested immunohistochemistry showed a larger number of accumulated Tregs in atherosclerotic plaques of Simvastatin-treated mice compared with controls. Furthermore, Foxp3 mRNA and protein levels in advanced atherosclerotic lesions were significantly increased /4

4/6 with Simvastatin therapy. The result showed that "Simvastatin promotes an accumulation of Tregs within the atherosclerotic plaques. Interestingly, we did not find a significant difference in serum levels of total cholesterol, triglycerides and LDL cholesterol with /5

5/6 and without Simvastatin in mice, which was consistent with the previous studies indicating that Simvastatin influenced the number of Tregs in plaques, independent of its lipid-lowering properties". /6

6/6 Statins also deplete vital biochemicals necessary for calcium homeostasis. Statins are Vitamin K antagonists. Paradoxically, statins increase the risk of increased calcium burden, leading to more advanced atherosclerosis.
pubmed.ncbi.nlm.nih.gov/25655639/