Gene helps prevent heart attack, stroke - and may offer way to block effects of aging

Don't worry, nothing will be done to follow this up for decades, not in time to help your children or grandchildren.
http://www.mdlinx.com/internal-medicine/medical-news-article/2016/05/26/6680593/?news_id=2386&newsdt=052816&subspec_id=1531&utm_source=WeeklyNL&utm_medium=newsletter&utm_content=Weeks-Best-Article&utm_campaign=article-section&category=latest-weekly

University of Virginia Health System News, 05/26/2016

A gene that scientific dogma insists is inactive in adults actually plays a vital role in preventing the underlying cause of most heart attacks and strokes, researchers at the School of Medicine have determined. The discovery opens a new avenue for battling those deadly conditions, and it raises the tantalizing prospect that doctors could use the gene to prevent or delay at least some of the effects of aging. “Finding a way to augment the expression of this gene in adult cells may have profound implications for promoting health and possibly reversing some of the detrimental effects with aging,” said researcher Gary K. Owens, PhD, director of UVA’s Robert M. Berne Cardiovascular Research Center. The researchers found that Oct4 controls the movement of smooth muscle cells into protective fibrous “caps” inside the plaques – caps that make the plaques less likely to rupture. The researchers also have provided evidence that the gene promotes many changes in gene expression that are beneficial in stabilizing the plaques. This is exciting, because studies suggest that it may be possible to develop drugs or other therapeutic agents that target the Oct4 pathway as a means to reduce the incidence of heart attacks or stroke. “Our findings have major implications regarding possible novel therapeutic approaches for promoting stabilization of atherosclerotic plaques,” said Olga A. Cherepanova, PhD, a senior research scientist in Owens’ lab. One surprising finding from UVA’s research: When the researchers blocked the effect of Oct4 in mice, they thought the atherosclerotic plaques might become smaller, because of the reduced number of smooth muscle cells inside. Instead, the plaques grew larger, less stable and more dangerous, stuffed with lipids, dead cells and other damaging components. The discovery was described in a paper published online by the journal Nature Medicine.