The calcification of arterial wall is an accumulation of calcium into blood vessel walls, which can frequently be a forecaster of severe cardiovascular incidents such as strokes and heart attacks. For long researchers have pointed to family medical history as one potential reason for solidifying the arteries, but the latest study issued in the journal Nature Genetics links the HDAC9 gene in the calcification of the human aorta, which is the largest blood vessel in the body. The study analyzed over 11,000 individuals and discovered patients having noteworthy blood vessel calcification were probably to have a particular variant of HDAC9.

This high-peril variant of HDAC9 is seen in about 25% of the population. In the mouse studies, the scientists discovered that HDAC9 caused unusual alterations in the cells of the vessel walls, similar to that of the bone cells in humans. Rajeev Malhotra—Study’s Co-Lead Author from the MGH (Massachusetts General Hospital) Cardiovascular Research Center—said, “Our research demonstrated HDAC9 is not just linked with cardiovascular disease but can, in fact, induce it by modifying the makeup of those vascular cells.” The researchers discovered that inhibiting HDAC9 in mice conserved normal function in vascular cells and averted vascular calcification, thus discovering HDAC9 as a goal for the promising treatment of cardiovascular disease.

On a similar note, recently, the research identified a cause of solidifying of the arteries and a latent treatment. A team of scientists from the U.K. identified the mechanism about a hardening of the arteries and shown in animal investigations that a generic medication usually utilized to cure acne can be a useful treatment for the condition. The research team from the University of Cambridge and KCL (King’s College London) discovered that a molecule once believed only to survive inside cells for repairing DNA is also accountable for solidifying of the arteries, which is linked with heart disease, dementia, stroke, and high blood pressure.