Stanford scientists have found a type of cell in a growing heart that could repair damaged coronary arteries.
Stanford scientists have found a type of cell in a growing heart that could repair damaged coronary arteries, a discovery that could lead to new heart disease treatments.
Coronary artery disease is the leading cause of death worldwide, but there is currently no effective method to regenerate new coronary arteries in diseased or injured hearts.
The findings identified a progenitor cell type that could make it possible.
The study was carried out with mice but, as the blood vessels of the human heart are similar, it could lead to new treatments for the disease or to restore blood flow after a heart attack, researchers said.
“Current methods to grow new blood vessels in the heart stimulate fine blood vessels rather than re-establishing the strong supply of blood provided by the main arteries. We need arteries to restore normal function,” said senior author Kristy Red-Horse from the Department of Biological Sciences at Stanford University.
“If we want to regenerate diseased hearts, we need to first understand how the heart creates the building blocks of healthy coronary arteries,” said lead author Dr Katharina Volz, from Stanford.
It was already known that smooth muscle is formed from cells in the epicardium, the layer that covers the heart. During embryonic development, many epicardial cells travel deeper into the wall of the heart and some form smooth muscle.
But the original cell type that undergoes this transition, and the signals that trigger differentiation into smooth muscle, were poorly understood.
The team can now show that the smooth muscle of the arteries is derived from cells called pericytes. The small capillary blood vessels throughout the developing heart are covered in pericytes.
They receive signals through a protein called Notch 3 to differentiate and form the smooth muscle covering needed for larger artery walls.
Pericytes are also found throughout the adult heart which suggests that they could be used to trigger a self-repair mechanism.
When the main arteries become blocked and a person suffers a heart attack, small collateral vessels can form a detour around the blockage. Large collateral arteries are required to provide significant blood flow to healing tissues.
Providing the right molecular signals to turn pericytes into smooth muscle cells may promote a transition from tiny blood vessels to true arteries in the healing heart.
The study was published in the journal eLife.
