101 research outputs found
Preferential uptake of radiolabeled oxidation-specific antibodies in lipid-rich versus collagen-rich lesions: Implications for noninvasive imaging of vulnerable plaques
IL-5 links adaptive and natural immunity specific for epitopes of oxidized LDL and protects from atherosclerosis
Influence of Maternal Dysmetabolic Conditions During Pregnancy on Cardiovascular Disease
Pathogenic factors associated with maternal hypercholesterolemia, obesity, and diabetic conditions during pregnancy influence fetal development and predispose offspring to cardiovascular disease. Animal models have established causeβeffect relationships consistent with epidemiological findings in humans and have demonstrated, in principle, that interventions before or during pregnancy can reduce or prevent pathogenic in utero programming. However, little is known about the mechanisms by which maternal dysmetabolic conditions enhance disease susceptibility in offspring. Identification of these mechanisms is rendered more difficult by the fact that programming effects in offspring may be latent and may require conventional risk factors and inherited genetic co-factors to become clinically manifest. Given the increasing prevalence of maternal risk factors, which is expected to lead to a wave of cardiovascular disease in the coming decades, and the length of prospective studies on developmental programming in humans, greater-than-usual emphasis on experimental models and translational studies is necessary
The fetal origins of atherosclerosis: maternal hypercholesterolemia, and cholesterolβlowering or antioxidant treatment during pregnancy influence in utero programming and postnatal susceptibility to atherogenesis
It takes three to tango: genes complicate the association between birth weight and cardiovascular disease.
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A Gut Feeling About Developmental Programming Mechanisms: Trimethylamine-N-Oxide May Enhance Atherosclerosis in Offspring of Hypercholesterolemic Mice.
Effect of maternal cardiovascular conditions and risk factors on offspring cardiovascular disease.
Maternal-fetal cholesterol transport in the placenta: good, bad, and target for modulation.
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