In a heart attack, a series of biochemical processes leave the heart damaged, much like a car after an accident. There is loss of tissue that needs to be rebuilt, proteins that get crushed, muscle damage, and interruptions to blood and oxygenflow to the heart. Because the heart is not very good at repairing itself, it is important to discover ways to minimize damage in the first place.
Researchers from San Diego State University’s Heart Institute discovered how one key protein in the heart can act as the knight in shining armor, reducing the damage from the attack, which could improve survival rates and heart function in those who do survive.
“The more your heart is damaged, the worse the long-term prognosis, so that’s where our research is focused,” said Chris Glembotski, molecular cardiologist and director of the SDSU Heart Institute.
“We study how to make the heart more resilient to the damage of a heart attack, which would improve patient’s recovery,” added Glembotski.
After an attack, many patients have stents put in to open up blocked arteries, which helps in the long term. But the surge of oxygen has drawbacks as well.
“The oxygen surge that occurs as soon as the stent is implanted ‘stuns’ the heart cells and some of them die, which increases irreparable damage to the heart. We found a protein that can minimize the stunning,” said Glembotski.
Glembotski and doctoral candidate Adrian Arrieta found that the protein, MANF (mesencephalic astrocyte-derived neurotrophic factor), acts much like an automobile collision specialist, correcting other proteins that have misfolded.
MANF is among roughly 20,000 proteins in the heart.
Immediately after a heart attack there is a ‘golden period’ when intervention to reduce the severity and damage can significantly boost chances of not only survival but also the level of functionality that the heart regains in recovery. (ANI)