Keio University

Discovery of Immune Cells Crucial for Tissue Repair and Reinforcement After Myocardial Infarction in a Mouse Model—A New Challenge for Innovative Therapies to Restore Cardiac Function—

Publish: July 03, 2018
Public Relations Office

July 3, 2018

Keio University School of Medicine

Associate Professor Motoaki Sano and Assistant Professor Kosuke Shirakawa of the Department of Cardiology, School of Medicine, Keio University, have discovered immune cells (osteopontin-producing macrophages) that are crucial for tissue repair and reinforcement after a myocardial infarction and have clarified the mechanism by which they differentiate.

Acute myocardial infarction is a disease in which the myocardium becomes necrotic due to a sudden blockage of the coronary arteries, the blood vessels that supply oxygen and nutrients to the heart muscle. Since myocardial cells cannot regenerate, if the myocardium in the infarcted area thins, the heart can no longer pump enough blood to the body, eventually leading to a condition called heart failure. Given these circumstances, it is believed that promoting the repair of damaged heart tissue, reinforcing the thinned myocardial tissue, and restoring cardiac function will lead to improved survival rates for patients with myocardial infarction.

Various immune cells gather at the site of a myocardial infarction. Among them, macrophages, a type of white blood cell, play a crucial role in wound healing. They have the ability to phagocytose (engulf) and remove the debris of destroyed tissue and then promote the synthesis of fibrous tissue materials like collagen to repair and reinforce the tissue.

In this study using mice, the researchers discovered that macrophages gathering in necrotic tissue phagocytose the debris of destroyed tissue by producing a substance called "osteopontin." Furthermore, they clarified the mechanism by which cells originating from the bone marrow differentiate into macrophages at the site of myocardial infarction and produce osteopontin.

The results of this research are expected to contribute to the development of innovative therapies that prevent the onset of heart failure by increasing osteopontin-producing macrophages in the infarcted tissue, thereby enhancing the patient's own healing power, promoting tissue repair and reinforcement after myocardial infarction, and restoring cardiac function.

These research findings were published in "Circulation," the top journal in the field of cardiology, on Monday, July 2, 2018 (U.S. Eastern Time).

*Note added on Tuesday, July 3, 2018: At the time of the press release distribution, publication was scheduled for Thursday, June 28, but this was changed to Monday, July 2.

For the full press release, please see below.

Press Release (PDF)