Atherosclerosis is an inflammatory condition. Oxidized lipids//en.wikipedia.org/wiki/Lipid_peroxidation”>Oxidized lipids lead to the formation of fatty plaques that narrow and weaken blood vessels, the growth of those plaques driven by the activities of macrophages that try and fail to repair the damage. They become overwhelmed and die: plaques are a mix of fat and the cellular debris from dead macrophages. Prior to their destruction, macrophages generate inflammatory signaling as atherosclerosis worsens, but how is it that other sources of age-related chronic inflammation can accelerate the progression of atherosclerosis? Researchers here explore some of the less well-understood parts of the feedback loop between inflammation and mechanisms of atherosclerosis, in search of answers.
Investigators have identified a new cellular pathway that may help explain how arterial inflammation develops into atherosclerosis – deposits of cholesterol, fats, and other substances that create plaque, clog arteries, and promote heart attacks and stroke. “We have known for decades that atherosclerosis is a disease of chronic inflammation that ultimately results in the scarring of arteries and tissue damage. But the ongoing stimulus for this inflammation has been unclear.”
A new study sheds light on this mystery by using a bacterial infection to reveal
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