Health
UCLA researchers identify protein important for healing after heart attack
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UCLA scientists have identified the protein GPNMB as a key regulator in the heart's healing process after a heart attack.
Using animal models, they demonstrated that bone marrow-derived immune cells called macrophages secrete GPNMB, which binds to the receptor GPR39 and promotes cardiac repair. These findings provide a new understanding of how the heart heals and could lead to new treatments aimed at improving heart function and preventing progression to heart failure.
background
Someone in the United States has a heart attack every 40 seconds – the leading cause of heart failure. These cardiac events weaken the heart and cause scarring that reduces the heart's ability to pump blood effectively. And although this scar tissue initially forms to maintain the structure of the heart, it remains permanently and strains the remaining muscles, eventually leading to heart failure.
Previous clinical studies have shown that GPNMB, or glycoprotein non-metastatic melanoma Protein B is strongly associated with cardiovascular disease outcomes in heart failure patients. What was not clear, however, was whether the lack of this protein was directly responsible for the development of heart failure after a heart attack. This important difference is – whether GPNMB is simply related or not biomarker or those that play a causal role – determine whether the protein can be considered a therapeutic target for future studies.
method
Using a mouse model, researchers established for the first time that GPNMB is not naturally expressed by the heart itself, but is produced by inflammatory cells derived from bone marrow. After a heart attack, these macrophages migrate to the injured site of the heart, where they express GPNMB.
The team performed a gene knockout -; inactivating the GPNMB gene -; [AS1] Mice lacking the GPNMB gene were observed to have dramatically worse outcomes after a heart attack, including a higher incidence of heart rupture, a fatal complication also seen in human heart failure patients. Conversely, additional administration of circulating GPNMB protein to mice with normal GPNMB expression improved cardiac function and reduced scarring. Four weeks after a simulated heart attack, 67% of animals lacking the GPNMB gene showed severe fibrosis or scarring, compared to only 8% of animals in the control group.
In addition to identifying GPNMB as a signaling molecule that affects a variety of cell types, the researchers discovered that GPNMB is a signaling molecule that affects a variety of cell types, as well as GPR39, a receptor previously thought to be an orphan receptor, or a receptor with unknown binding partners. I discovered that it connects. This interaction triggers a cascade of signals that promote tissue regeneration and limit scarring.
impact
Cardiovascular disease – Heart failure is a terminal complication – It is a serious health problem and accounts for approximately one-third of deaths worldwide. Despite its prevalence, there are no treatments that directly increase the heart's ability to repair itself after a heart attack. New research demonstrates the potential of GPNMB as a therapeutic agent as well as GPR39 as a target that can limit scarring, improve heart function and prevent heart failure.
This study may also have far-reaching implications for our understanding of tissue repair in other organs. Because GPNMB is expressed in multiple tissues, future studies will investigate its role in repairing the brain, kidney, and other organs affected by ischemic injury.
sauce:
Reference magazines:
Ramadoss, S. others. (2024). Bone marrow macrophage-derived GPNMB protein binds to the orphan receptor GPR39 and plays an important role in cardiac repair. Nature cardiovascular research. doi.org/10.1038/s44161-024-00555-4.
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