Therapeutic angiogenesis has been found to aid in cardiac bypass, making surgery unnecessary. Coronary artery disease
is one of the most common heart disease, it leads to thickening of the arteries and restricts the flow of blood. This occurs due to the accumulation of cholesterol in the blood vessels called plaque. The build up of plaques in the blood vessel is called atherosclerosis.
‘AGGF1 protein to beat heart blocks.
increases, the amount of blood reaching the heart is reduced, leading to poor heart function. Sudden stoppage of blood flow to the heart can lead to a heart attack.
- Coronary artery disease is the most common type of heart disease.
- It kills nearly 380,000 in the U.S every year.
- Every 34 seconds someone has a heart attack
- Every 60 seconds someone dies of a heart related disease.
Qing Kenneth Wang and colleagues studied the effect of AGGF1, a protein that aids in angiogenesis, with their paper published in the Journal PLOS biology
. The scientists have used
Response in Human Endothelial Cells
- AGGF1 to promote the formation of new blood vessels.
- Normal process of autophagy that removed cellular structures that are damaged. The molecular components from these structures are then utilized.
The researchers studied the effect of AGGF1 on endothelial cells. It was found that AGGF1 induced autophagy in these endothelial cells. The autophagy was identified by the detection of markers as well as changes noticed in the endothelial cells. AGGF1 in Mice
The researchers studied the effect of AGGF1 on the heart of mice and found that not only endothelial cells, but all cell types were influenced by the presence of this protein. Endothelial Cells with Drugs that Block AGGF1
Endothelial cells that were treated with drugs that blocked AGGF1 were studied to examine the connection between autophagy and angiogenesis. The endothelial cells showed signs of early blockage to the growth of new blood vessels. This suggests that AGGF1 mediated autophagy was required for angiogenesis. Mice with Mutation in One or Both AGGF1 Gene
Mice with Myocardial Infarction
- Mice with no AGGF1 died in the embryo stage
- Mice with one copy of AGGF1 gene survived till they reached adulthood. The amount of autophagy in the heart was reduced.
Mice heart after myocardial infarction was found to have an increase in the amount of AGGF1. This could be due to hypoxic condition that prevails in the region after a myocardial infarction.
When some of the mice were injected with additional AGGF1, their recovery was better, with more number of mice surviving 2 weeks and 4 weeks after the incident. The echocardiograms of the mice that received additional AGGF1 were also much better than mice that did not receive additional AGGF1.
Highlights of the Study
- AGGF1 induces both autophagy and angiogenesis
- The protein increases the number of cardiac cells that survive after myocardial infarction compared with mice that did not receive external injection of the protein after myocardial infarction.
- A molecular regulator called JNK was identified during the study that mediates the activity of AGGF1.
The study provides an insight into key mechanisms that play a pivotal role in recovery after myocardial infarction, offering potential for a novel method of treatment of heart blocks without the need for surgery. References:
- Heart statistics - (https://www.bhf.org.uk/research/heart-statistics)
- Heart Disease: Scope and Impact - (http://www.theheartfoundation.org/heart-disease-facts/heart-disease-statistics/)