During a heart attack, the heart is starved of oxygen and heart muscle is damaged. The body responds by sending in immune cells to clear up dead and dying cells, but these cells themselves cause further inflammation in the already damaged heart, and this can lead to heart failure.
Researchers from the University of Oxford in the UK found that injecting a protein called VEGF-C after heart attacks in mice significantly reduced the amount of damaged heart muscle, and allowed the heart to recover almost all of its pumping function.
In comparison, untreated mice lost almost half of their heart function after a heart attack.
The VEGF-C treatment promoted growth of a network of vessels which are part of the lymphatic system.
The study, published in the Journal of Clinical Investigation, showed that the extra lymphatic vessels allow the immune cells to be quickly cleared after helping to repair and clear dying and dead cells, but before they can cause significant damage from inflammation.
This treatment led to better healing in the heart and better recovery of the heart's pumping function after a heart attack.
When the heart's ability to use the lymphatic system to clear away the immune cells was hampered, more scarring developed, the muscle could not pump as well, and the whole heart started to change shape in response to the damage.
Researchers believe that by clearing away macrophages, the first line of immune cells that start the healing process, other immune cells called Tregs could then be allowed into the injured muscle, to further help the heart to repair and recover.
Future research and treatments will focus on achieving the best balance of immune cells after a heart attack to ensure initial heart repair doesn't escalate to inflammation, scarring and heart failure.
BHF Professor of Regenerative Medicine leads the BHF Centre of Regenerative Medicine in Oxford and Cambridge and led the research. He said:
"We started looking at the lymphatic system in the heart a few years ago - we could never have known how pivotal it might turn out to be for heart repair," said Paul Riley, of British Heart Foundation.
"We now know that it's not enough to just get healing immune cells into the heart. We need to boost the routes that remove these immune cells once they've done their job, so that they don't start causing more harm and ultimately contribute to the long-term damage that leads to heart failure," said Riley.
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