Triggering the body to produce new blood vessels could prove an alternative to bypass surgery in the treatment of coronary artery disease
With heart disease topping the charts as the number one killer worldwide, we are in dire need of new therapies to both prevent and fix any damage caused by impaired blood flow. One contender therapy is angiogenesis – the creation of new blood vessels by endothelial cells.
How can we trigger angiogenesis?
Applying factors signals the body to form new blood vessels, and one such protein factor is AGGF1. AGGF1 works by signalling endothelial cells to form new blood vessels, but in doing so it also initiates a process called autophagy. Autophagy translates as ‘self-eating’, and stands for a recycling process that breaks down old material to make way for the new. Autophagy is an important process in longevity, as increased autophagy improves quality control by wiping away more old, decrepit proteins. Applying AGGF1 has been shown to be an effective treatment for heart attacks in mice, and when researchers analysed its effects further they found that not only was it signalling angiogenesis; it was also triggering autophagy in a range of other cells too.
The connection between autophagy and angiogenesis
When the research team used autophagy inhibiting drugs to monitor this relationship, they found it blocked blood vessel formation – hinting that autophagy is an essential component of angiogenesis following AGGF1 exposure. When they then looked at mice with mutations in the AGGF1 gene, they found that mice with mutations in both copies died before birth. Mice with one functional copy survive, but crucially have a reduced level of autophagy in their heart tissue.
When they tested AGGF1 on a mice heart attack model, they found it extended the period of autophagy following such an event and improved survival rates, as well as reducing scar formation too. While this is still early days, and the influence of autophagy on angiogenesis isn’t entirely unravelled, it suggests application of factors such as AGGF1 could be an additional strategy to improve survival – boosting both autophagy and angiogenesis at the same time.
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