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.
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