AGGF1 is an “angiogenic factor” that promotes the proliferation of endothelial cells, the thin layer of cells that line the inner surface of blood vessels. In initial experiments, scientists saw that this protein relies on autophagy, a self-degradative process the body uses to balance sources of energy “at critical times in development and in response to nutrient stress, for effective blood vessel formation.
Researchers also experimented with removing one or both copies of the AGGF1 gene in mice. Mice without either copy of the gene didn’t make past the embryonic stage. Sixty percent of the mice with only one copy did survive to adulthood, but they showed reduced levels of autophagy and subsequently reduced angiogenesis in their hearts.
Lastly, researchers also looked at the levels of AGGF1 in a mouse model of myocardial infarction (heart attack). Levels of AGGF1 drastically increased in the parts of the heart damaged by a lack of oxygen supply after the attack. However, treating these mice with exogenous AGGF1 increased the amount of mice models that survived two and four weeks after heart attack, as well as improved other measurements relating to heart health.
There’s still a wide gap to fill between what scientists know for sure about AGGF1 and myocardial infarction in mice and the same condition in humans, but the potential depicted by this study’s results represent a truly promising future for reducing the invasiveness of post-heart attack medical care.
Sources: PLOS, NCBI, American Heart Association, The Journal of Pathologies