Gene Drug Therapy for Myocardial Infarction

The gene drug therapy can treat myocardial infarction.
Reporter recently learned from the United Nations International Center for Genetic Engineering and Biotechnology (ICGEB) that its research team has developed a new type of therapy, which can help to induce cardiac cell regeneration and treat heart failure by implanting gene drugs. Myocardial infarction is a kind of coronary heart disease with coronary atherosclerosis. The sudden obstruction of coronary artery leads to ischemia and necrosis of myocardial cells. Permanent structural damage of myocardial infarction site increases the risk of heart failure, which is very serious and can directly cause death. According to the World Health Organization, the disease has affected more than 23 million people in the world.
This is the first experiment to prove that heart regeneration can be achieved by implanting effective gene drugs. The drug stimulates heart regeneration in large animals, which has the same cardiac structure and physiological functions as humans. According to Professor Maro Gaka, the first author of the article and head of the research team, the experiment used a virus to deliver microRNA molecules to infarcted heart cells. In large mammals, cardiac repair can be achieved by strictly controlling therapeutic agents to stimulate the proliferation of endogenous cardiomyocytes. But at present, the dosage and time of administration can not be effectively controlled. In the long run, adverse reactions will occur. Gaca added: "Although we know that this works well in mice, clinical trials in large mammals will take a while to proceed, and we need to learn how to manage RNA as a synthetic molecule in large animals and patients."
Gaka said: “This is a very exciting moment. After several failed attempts to regenerate the heart with stem cells, we first saw real heart repair. The study was completed by ICGEB in collaboration with the Santa Ana Institute of Higher Education in Italy and the Monastario Foundation Hospital. ”
2026-09-06
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