Hypercholesterolemia and inflammation in atherogenesis: two sides of the same coin.

摘要: An abundance of experimental, clinical, and epidemiologic data capped by stunning interventional results with the statins has established hypercholesterolemia as a major causative factor in atherogenesis. In familial animal models it is sufficient cause. Some degree hypercholesterolemia, perhaps 30–50 mg/dL, may even be necessary It equally clear that from very beginning atherogenesis strong inflammatory component, i. e., characterized penetration monocytes T-cells into developing lesion. These cells, through secretion cytokines growth factors, immune responses, complex cross-talk elements artery wall modulate lesion affect its stability. But inflammation to occur response something. What something? “injury” “response-to-injury”? The case will made oxidized lipids LDL or generated prooxidative changes cells should considered plausible candidate. There no need consider alternative hypotheses. Both are much involved. Optimal intervention prevention probably require attention both.