Researchers at Yale School of Medicine have discovered a protein called macrophage migration inhibitory factor (MIF) that influences the cardiac response to the loss of blood flow and oxygen to the heart.
The study revealed that the protein activated an imperative cellular stress response enzyme called AMP-activated protein kinase (AMPK), which monitored cellular energy balance and shielded from heart attack injury.
Dr Richard Bucala, co author and professor of rheumatology and pathology who co-authored the study said that the protein was discharged in response to oxygen deprivation activated AMPK.
"We found that when MIF is released in response to a lack of oxygen, it causes the activation of AMPK," said Nature quoted Dr. Bucala, as saying.
"Thus, this protein which contributes to inflammatory diseases has a protective metabolic effect in the heart," he added.
The study, conducted using a mice model, found that the mice short of the MIF gene lacked AMPK response and experienced more severe heart attacks than mice with an intact MIF gene.
Researchers said that a common variation in the MIF gene in people also to reduces the levels of MIF protein expression.
The findings also showed that cells from people with this genetic variant also have less activation of AMPK that might boost the risk of cardiac injury during a heart attack.
"This suggests that we might be able to identify individuals, based on their genetic characteristics, who are likely to suffer more cardiac damage during a heart attack," said senior author Lawrence Young, M.D., professor of cardiovascular medicine, and physiology.
The team believes that the findings may lead to developing new therapies to treat the loss of blood flow and oxygen to the heart.
The study appears in Journal Nature.