ANGPTL2 Accelerates Heart Disease Development

Genetically engineered loss of ANGPTL2 has been shown to slow the progression of heart disease in mice. Lower levels of ANGPTL2 result from exercise, and higher levels are associated with greater age, greater amounts of visceral fat, and the presence of senescent cells, among other factors - all of which fits well with the range of known risk factors for heart disease. The more ANGPTL2 in circulation, the worse the outcome. This open access review paper covers what is presently known of ANGPTL2 and its role in metabolism and age-related cardiovascular disease: of interest given the past few years of research is that ANGPTL2 may be generated by senescent cells as a part of their harmful senescence-associated secretory phenotype. Worldwide, the number of patients with heart disease is increasing as populations of elderly people expand. Of the heart diseases, cardiovascular disease (CVD) and heart failure (HF) are associated with adverse health outcomes that decrease a patient's well-being and productivity. Prevention of these conditions is desirable to promote healthy aging and improve patients' lifestyle. The pathologic basis of CVD is atherosclerosis caused by ectopic accumulation of cholesterol in vessel walls; thus advent of therapies aimed at reducing low-density lipoprotein (LDL)-cholesterol levels has succeeded in decreasing the number of CVD events. However, these events continue to occur, even in patients whose LDL-cholesterol levels have been lowered, indicat...
Source: Fight Aging! - Category: Research Authors: Tags: Daily News Source Type: blogs