Endothelial cells may contribute to formation of new vessels compensating for inadequate blood supply
Circulation Research Journal Report
Embargoed until 4 a.m. CT / 5 a.m. ET Monday, Jan. 22, 2018
DALLAS, Jan. 22, 2018 – Cells that line the interior surface of blood vessels (endothelial cells) have the capacity to clonally expand and contribute to the development of new vessels due to inadequate blood supply to the heart, known as ischemia, according to a study in mice published in Circulation Research, an American Heart Association journal.
“There are numerous areas within and beyond cardiovascular medicine, where the ability to increase endothelial growth in a controlled manner would be of significant clinical value,” said Circulation Research editor Roberto Bolli. M.D.
Bolli is Chief of the Division of Cardiovascular Medicine and Director of the Institute of Molecular Cariology at the University of Louisville in Kentucky.
“Attempts to control endothelial growth and proliferation for therapeutic gain, in the areas of coronary artery and peripheral vascular disease, have been met with limited success,” he said. “These data provide potentially important information that endothelial proliferation, a critical process for meeting this goal, does not occur at random, but rather is the result of selective cells providing a greater than random contribution to the total new vasculature.”
The study’s senior author is Stefanie Dimmeler, Ph.D., Director of the Institute for Cardiovascular Regeneration Centre of Molecular Medicine at Goethe University Frankfurt in Frankfurt, Germany
The study was funded the Excellence Cluster Cardiopulmonary Systems (German Research Foundation), and the LOEWE Centre for Cell- and Gene Therapy (State of Hesse) and the German Research Foundation (SFB834). The authors declare no competing financial interests.
- After Jan. 22, 2018, view the manuscript online.
- Follow AHA/ASA news on Twitter @HeartNews
- For updates and new science from the Circulation Research journal follow @CircRES.
Statements and conclusions of study authors published in American Heart Association scientific journals are solely those of the study authors and do not necessarily reflect the association’s policy or position. The association makes no representation or guarantee as to their accuracy or reliability. The association receives funding primarily from individuals; foundations and corporations (including pharmaceutical, device manufacturers and other companies) also make donations and fund specific association programs and events. The association has strict policies to prevent these relationships from influencing the science content. Revenues from pharmaceutical and device corporations and health insurance providers are available at www.heart.org/corporatefunding.
About the American Heart Association
The American Heart Association is devoted to saving people from heart disease and stroke – the two leading causes of death in the world. We team with millions of volunteers to fund innovative research, fight for stronger public health policies and provide lifesaving tools and information to prevent and treat these diseases. The Dallas-based association is the nation’s oldest and largest voluntary organization dedicated to fighting heart disease and stroke. To learn more or to get involved, call 1-800-AHA-USA1, visit heart.org or call any of our offices around the country. Follow us on Facebook and Twitter.
For Media Inquiries and AHA/ASA Spokesperson Perspective: 214-706-1173
Bridgette McNeill: 214-706-1135; firstname.lastname@example.org
For Public Inquiries: 1-800-AHA-USA1 (242-8721)