Researchers from King’s College London have find that therapy that can induce heart cells to regenerate after a heart attack. Myocardial infarction, more commonly known as a heart attack, cause by the sudden blocking of one of the cardiac coronary arteries, is the main cause of heart failure, a condition that now affects over 23 million population in the world, according to the World Health Organisation.
Genetic material into cells
Gene therapy is design to introduce genetic material into cells to compensate for abnormal genes or to make a beneficial protein. If a mutate gene causes a necessary protein to be faulty or missing, gene therapy may be able to introduce a normal copy of the gene to restore the function of the protein.
A gene that is insert directly into a cell usually does not function. Instead, a carrier called a vector is genetically engineer to deliver the gene. Certain viruses are often use as vectors because they can deliver the new gene by infecting the cell. At present, when a patient survives a heart attack; so they are left with permanent structural damage to their heart through the formation of a scar; which can lead to heart failure in the future.
In contrast to fish and salamander, which can regenerate the heart throughout life. In this study, published today in Nature; so the team of investigators delivered a small piece of genetic material; so called microRNA-199, to the heart of pigs, after a myocardial infarction; which result in the almost complete recovery of cardiac function at one month later.
Heart using stem cells
Lead author Professor Mauro Giacca, from King’s College London said: “It is a very exciting moment for the field. After so many unsuccessful attempts at regenerating the heart using stem cells; which all have failed so far, for the first time we see real cardiac repair in a large animal. However, subsequent persistent and uncontroll expression of the microRNA resulted in sudden arrhythmic death of most of the treated pigs.
Such events were concurrent with myocardial infiltration of proliferating cells displaying a poorly differentiate myoblastic phenotype. These results show that achieving cardiac repair through the stimulation of endogenous cardio myocyte proliferation is attainable in large mammals, however dosage of this therapy needs to be tightly controlled.
This is the first demonstration that cardiac regeneration can be achieved by administering an effective genetic drug that stimulates cardiac regeneration in a large animal, with heart anatomy and physiology like that of humans. It will take some time before we can proceed to clinical trials explained Professor Giacca. They still need to learn how to administer the RNA as a synthetic molecule in large animals and then in patients; but they already know this works well in mice.