Atherosclerosis is the progressive buildup of plaque - the fatty deposits and other cells - in the inner walls of the arteries. The condition is a consequence of elevated cholesterol and for many it's a silent disease, with no visible signs or symptoms. The disease can begin in early adulthood and continues to progress for the rest of a person's life. Despite the serious nature of atherosclerosis, many people do not understand how it develops and progresses.
A group at the Centro Nacional de Investigaciones Cardiovasculares (CNIC), collaborating with institutions in the USA, has shown that acquired mutations in the gene encoding the protein p53 contribute to the onset of atherosclerotic cardiovascular disease.
Mitochondria are generally known as the powerhouse of the cell, however, growing research indicates that they may potentially be involved in inflammation.
On July 25th, 2022, a new study perspective called “SLFN11’s surveillance role in protein homeostasis” was published in Volume 9 of Oncoscience.
Macrophages travel through our arteries, gobbling fat the way Pac-man gobbled ghosts. But fat-filled macrophages can narrow blood vessels and cause heart disease.
Insufficient oxygen to an area like the heart or legs, called hypoxia, is a cue to our bodies to make more blood vessels, and scientists have found some unusual partners are key to making that happen.
Scientists at the Centro Nacional de Investigaciones Cardiovasculares have identified a nuclear import mechanism essential for organ growth and development. Manipulation of this mechanism has potential applications in the control of organ growth and organ regeneration.
Scientists identified two blood proteins that positively influence human health and lifespan.
An artery is not like a nose. Or is it? Scientists at La Jolla Institute for Immunology (LJI) have discovered that immune cells in arteries can "sniff" out their surroundings and cause inflammation.
Up to 60 percent of the risk associated with coronary arteriosclerosis may be explained by changes in the activity of hundreds of genes working together in networks across several organs in the body.
Up to 60 percent of the risk associated with coronary arteriosclerosis may be explained by changes in the activity of hundreds of genes working together in networks across several organs in the body.
Professor Yuichi Oike and his group of researchers recently produced a peptide vaccine that mitigates conditions of dyslipidemia.
Food and beverages may have important effects on kidney health, but the potential biological mechanisms involved are often unclear.
Tiny synthetic particles known as dendrimers have been shown to avoid detection by our immune system and so could be used to develop a new system to deliver drugs into the body without triggering a reaction.
A high-fat diet disrupts the biology of the gut's inner lining and its microbial communities -; and promotes the production of a metabolite that may contribute to heart disease, according to a study published Aug. 13 in the journal Science.
Recent research discovered DNA signatures linked to the risk for cardiovascular disease, a breakthrough that can lead to opportunities for clinical interventions
Scientists from the University of Illinois Chicago (UIC) have found that heparanase (HPSE) is an important regulator of innate defense mechanisms of cells.
Carrots are a good source of beta-carotene, which is a precursor of vitamin A. But to get the full health benefits of this superfood, you need an active enzyme to produce this vitamin.
Researchers at the University of Virginia have shed light on how our genes affect our risk for coronary artery disease, the most common form of heart disease.
Tissues and cells in the human body are subjected to a constant push and pull - strained by other cells, blood pressure and fluid flow, to name a few.
High cholesterol kills. In fact, one in four Americans will die from the consequences of atherosclerosis, the buildup of plaques of fat and cholesterol in the arteries. Statins have helped reduce mortality, but millions are still at risk.