Recently, Professor Zeng Chunyu and Professor Wu Gengze from the Department of Cardiology of the Army Characteristic Medical Center (Daping Hospital) of the Army Military Medical University successfully found a new protein in the blood vessel, named it "angiosin", and confirmed that "angiosin" can lead to vascular remodeling through "transcript protein double action". The research results were published online recently in Circulation Research, a top international journal of basic research on cardiovascular diseases. Vascular remodeling and phenotype conversion of vascular smooth muscle cells are the main pathological processes of atherosclerosis and other vascular diseases, which can not only lead to hypertension, coronary heart disease, stroke, but also an important reason for vascular restenosis after stent implantation. Although researchers in cardiovascular, cerebrovascular, endocrine, tumor and many other disciplines have tackled key problems for decades, the veil of vascular remodeling has not been completely uncovered, which has seriously affected the prevention and treatment of related diseases. Zeng Chunyu and Wu Gengze's team have been devoted to the research on vascular remodeling of hypertension for many years. When detecting the gene expression in the aorta of hypertensive rats, they found a segment of long chain non coding RNA (lncRNA) with significantly increased expression in the vascular remodeling of hypertension. Through a series of studies on clinical specimens, gene editing animals and cells, the team found that this lncRNA can change the function of vascular smooth muscle cells from a healthy "contractive" type to an unhealthy "proliferative" type. Non coding RNA refers to RNA that does not encode proteins. This lncRNA discovered by the team may have the ability to encode proteins. Through rigorous verification, the team found the new protein "angiosin" for the first time in the world, and proved that "angiosin" can work cooperatively with its maternal lncRNA, aggravate vascular remodeling, and accelerate the progress of hypertension, coronary heart disease, stroke and other diseases. The team used a series of methods to knock out "angiosin" and its mother lncRNA in mice, and was surprised to find that the vascular remodeling of mice was effectively inhibited, the vascular thickening was significantly reduced, and the vascular elasticity was restored. Zeng Chunyu said that the new protein "angiosin" discovered and named by the team is expected to become a new therapeutic target for vascular remodeling related diseases. (Outlook New Times)