Researchers at the University of California, Los Angeles (UCLA) have identified a new role for the GPNMB protein in the heart’s healing process after a heart attack.
This finding, published in ‘Nature Cardiovascular Research’, could open doors for the development of treatments aimed at preventing heart failure in patients who have suffered a heart attack.
Using animal models, the researchers demonstrated that macrophagesimmune cells originating in the bone marrow, secrete GPNMB, which binds to the GPR39 receptor and promotes heart repair. This has allowed us to understand how cardiac tissue can regenerate and offers a possible therapeutic route to slow the progression towards heart failure, a problem that affects millions of people around the world.
Heart attacks represent the most common cause of heart failure in almost everyone. These events cause permanent scarring of the heart, which decreases its ability to pump blood.
Although scar tissue helps maintain the initial structure, its long-term presence forces the heart to exert extra effort, which, over time, leads to heart failure.
Previous studies have associated GPNMB with adverse cardiovascular outcomes, but it was unclear whether its deficiency could be the cause of heart failure after a heart attack, a critical finding in determining whether GPNMB may be a viable therapeutic target.
Less scar
Through experiments with mice, scientists verified that GPNMB is not produced in the heart naturally, but is expressed by inflammatory cells in the bone marrow that migrate to the damaged area after a heart attack. Deletion of the GPNMB gene in mice dramatically increased the incidence of post-infarction cardiac rupture, a serious complication also seen in humans. In contrast, those with normal levels of GPNMB and who received additional doses of the protein showed improved heart function and less scarring.
Additionally, GPNMB was found to act on the GPR39 receptor, initiating a chain of signals that limits scar formation and promotes tissue regeneration.
Heart failure and other cardiovascular diseases account for almost a third of global deaths. Currently, there are no treatments capable of improving heart regeneration after a heart attack. This study suggests that GPNMB and the GPR39 receptor could become therapeutic goals to reduce scarring and improve heart function.
Furthermore, since GPNMB is expressed in multiple tissues, future studies will explore its role in the repair of other organs, such as the brain and kidneys, in cases of ischemic injury.
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