Atherosclerosis

…and platelet biology interact in atherosclerosis; how physiology and patient outcomes can guide coronary revascularization; and how stem cells and biomaterials could produce living vascular replacements for congenital heart disease. Other discussions address cardiovascular gene therapy, precision medicine, trial design and causal inference, cardiometabolic disease, and the ro

Hyperlipidemia is a risk factor for developing atherosclerosis and neurodegenerative disorders, however the underlying molecular mechanisms are not well understood. Protein Kinase R-like Endoplasmic Reticulum Kinase (PERK) signaling is one of the molecular pathways thought to be involved in hyperlipidemia-driven neurodegeneration. Studies indicate that mitophagy, regulated by phosphatase tension homolog-induced kinase-1 (PINK1) and Parkin, is crucial for removing damaged mitochondria; otherwise, this can lead to disrupted mitochondrial function. Increased cholesterol levels impair mitophagy in

Atherosclerosis is the underlying cause of major cardiovascular events, including heart attack and stroke. The build-up of plaque in coronary arteries can be a major risk for events, but risk is significantly higher in patients with vulnerable rather than stable plaque. Diagnostic imaging of vulnerable plaque is extremely useful for both stratifying patient risk and for determining effectiveness of experimental intervention in reducing cardiovascular risk. In the preclinical setting, being able to distinguish between stable and vulnerable plaque development and pair this with biochemical measu

…Atherosclerosis – the hardening of arteries as we age – may predispose to stroke by triggering the formation of blood clots that block the blood supply to the brain, but also involves inflammation that may cause chronic damage