Novel gene therapy that protects ischemic myocardium in mouse model may limit myocardial loss following acute infarction

A novel gene therapy that responds specifically to ischemic myocardial cells may eventually protect human patients against further myocardial loss following an acute infarction, according to an article in the April issue of Hypertension.

The American research team designed an oxygen-sensitive biosensor that triggers expression of protective genes when myocardium becomes ischemic and inhibits expression after adequate blood flow has been restored. The research technique, which was tested in mice, minimized further injury after an acute myocardial infarction.

The molecular sensor contains both a means to increase the expression of protective heme oxygenase-1 (HO-1) genes and an oxygen-sensitive switch that can turn off expression after ischemic conditions ease. In the experiments, researchers injected this molecule directly into the hearts of mice one hour after the mice had an acute myocardial infarction.

Ten days following their infarctions, mice that received the biosensor-regulated gene therapy showed less myocardial scarring and better recovery of ventricular function than control mice injected with saline only. The researchers demonstrated with molecular techniques that turning on expression of the protective HO-1 genes prevented further myocardial cell infarction, limiting the area of damage.

Two of the researchers, M. Ian Phillips, PhD, DSc and Yao Liang Tang, MD, envision administering such therapy to patients after a first myocardial infarction to limit damage and prevent future infarctions. While much work remains to test and refine such a therapy, Phillips said that the new concept might eventually be an alternative to stents and bypass surgery.

“Repeated bouts of myocardial ischemia cause cumulative tissue damage in the heart vessels that can lead to a fatal heart attack,” said Phillips. “Therefore, what patients need is a gene therapy strategy that acts in the heart and switches on or off, so that the therapeutic protein is produced only where and when it is needed.”

“One of the exciting aspects of the approach, described by Tang et al, is the ability to directly link expression of potentially therapeutic genes to a pathological stimulus associated with myocardial infarction, ischemia,” stated an editorial in Hypertension. “Ultimately, this area of research will pave the way for development of ‘smart’ therapies for the heart that allow for early and rapid treatment of a wide variety of cardiac ailments.”




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