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<td><span style="font-family:Helvetica, sans-serif; font-size:20px;font-weight:bold;">NIH Director's Blog Daily Digest (Unofficial)</span></td>
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<td><a href="https://directorsblog.nih.gov/2024/11/14/discovery-of-culprit-behind-scars-in-heart-failure-points-to-possible-treatment-target/" style="font-family:Helvetica, sans-serif; letter-spacing:-1px;margin:0;padding:0 0 2px;font-weight: bold;font-size: 19px;line-height: 20px;color:#222;">Discovery of Culprit Behind Scars in Heart Failure Points to Possible Treatment Target</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Nov 14th 2024, 10:00</div>
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<p><figure class="wp-block-image size-large"><img fetchpriority="high" decoding="async" width="1024" height="576" src="https://directorsblog.nih.gov/wp-content/uploads/2024/11/IL-1-and-fibroblasts-in-heart-1.1-1024x576.jpg" alt="IL-1 dots fly into a scene of cardiac muscle. The muscle in the distance has fibroblast covered with IL-1 and is covered with fibers. In the foreground a fibroblast is protected by antibodies and the muscle has no fibers." class="wp-image-26640" srcset="https://directorsblog.nih.gov/wp-content/uploads/2024/11/IL-1-and-fibroblasts-in-heart-1.1-1024x576.jpg 1024w, https://directorsblog.nih.gov/wp-content/uploads/2024/11/IL-1-and-fibroblasts-in-heart-1.1-300x169.jpg 300w, https://directorsblog.nih.gov/wp-content/uploads/2024/11/IL-1-and-fibroblasts-in-heart-1.1-150x84.jpg 150w, https://directorsblog.nih.gov/wp-content/uploads/2024/11/IL-1-and-fibroblasts-in-heart-1.1-768x432.jpg 768w, https://directorsblog.nih.gov/wp-content/uploads/2024/11/IL-1-and-fibroblasts-in-heart-1.1-1536x864.jpg 1536w, https://directorsblog.nih.gov/wp-content/uploads/2024/11/IL-1-and-fibroblasts-in-heart-1.1-180x100.jpg?crop=1 180w, https://directorsblog.nih.gov/wp-content/uploads/2024/11/IL-1-and-fibroblasts-in-heart-1.1.jpg 1920w" sizes="(max-width: 1024px) 100vw, 1024px"></figure>
<p class="has-small-font-size"><em>Researchers identified a type of fibroblast cell (white) that helps form scar tissue after heart injury in response to an inflammatory signal called IL-1 (blue). Their research in mice suggests blocking this signal with monoclonal antibodies (purple) could reduce scarring and improve heart function.</em> <em>Credit: Donny Bliss/NIH</em></p>
<p>More than 6 million adults in the U.S. have <a href="https://www.nhlbi.nih.gov/health/heart-failure" target="_blank" rel="noreferrer noopener">heart failure</a>, a condition that develops when the heart can’t pump enough blood to meet the demands of the body. While lifestyle changes and treatment can slow heart failure, there’s no cure. One reason is that heart failure and other heart conditions including heart attacks lead heart muscle to become thickened and scarred in a process known as fibrosis. Effective strategies to reverse or stop fibrosis in the heart or other organs after injury, as is needed for recovery, have remained elusive.</p>
<p>Now, a new NIH-supported study offers a step forward in better understanding what happens in human heart failure. These findings, reported in <a href="https://www.nature.com/articles/s41586-024-08008-5" target="_blank" rel="noreferrer noopener"><em>Nature</em></a>, identify a cell type that may be a main culprit in the formation of scar tissue after heart injury. What’s even more encouraging is that the study, which included mouse models, suggests that existing treatments that block communication between the immune system and the scar-forming cells may hold promise for limiting fibrosis to improve heart function.</p>
<p>These new findings come from a team led by <a href="https://profiles.wustl.edu/en/persons/kory-lavine" target="_blank" rel="noreferrer noopener">Kory Lavine</a> at Washington University School of Medicine, Saint Louis. The researchers set out to get a more detailed view of how immune and fibroblast cells may drive fibrosis in the failing human heart. <a href="https://www.genome.gov/genetics-glossary/Fibroblast" target="_blank" rel="noreferrer noopener">Fibroblasts</a> are connective tissue cells that make collagen and other fibrous materials that support and connect our tissues and organs. Fibroblasts also play an important role in wound healing, including through the formation of scars.</p>
<p>The heart contains many different types of fibroblasts, each with different roles. Some support the heart’s structure and maintain blood flow through the heart’s blood vessels, while others spring to action after injury to drive inflammation and the formation of scar tissue. The researchers investigated which fibroblasts were which by sequencing RNA within single cells, as well as by using other methods. They examined heart tissue taken from 45 individuals including healthy donors, people who recently had heart attacks, and people with heart failure. After determining differences among fibroblast cell types in the healthy and injured human hearts, the researchers identified one type of fibroblast cell in the heart as an important driver of fibrosis in heart failure.</p>
<p>To learn more, they tested mouse models of heart failure, and found one that included fibroblasts that closely resembled what they’d seen in the human samples. They then identified an inflammatory signal called IL-1 beta that plays an important role in driving the fibroblasts to produce scar tissue in the mice. This suggested that treatments to block IL-1 beta might thwart communication signals from the immune system to the fibroblasts to reduce scarring.</p>
<p>To test this, the researchers used an existing monoclonal antibody, a lab-produced protein that can be used as a treatment to modulate the immune system, that targets IL-1 beta. They found this treatment could reduce scarring in mouse heart tissue and improve the pumping ability of the heart. The finding is especially promising because therapies that block IL-1 signals are already approved by the Food and Drug Administration (FDA) to treat inflammatory conditions including <a href="https://www.niams.nih.gov/health-topics/juvenile-arthritis" target="_blank" rel="noreferrer noopener">juvenile idiopathic arthritis</a> and recurrent <a href="https://www.nhlbi.nih.gov/health/heart-inflammation/pericarditis" target="_blank" rel="noreferrer noopener">pericarditis</a>, a condition in which the sac surrounding the heart becomes inflamed.</p>
<p>Interestingly, the researchers noted that findings from a clinical trial testing an antibody that blocks IL-1 beta to help with <a href="https://www.nhlbi.nih.gov/health/atherosclerosis" target="_blank" rel="noreferrer noopener">atherosclerosis</a>, or plaque buildup in the arteries, have suggested the treatment might lead to a reduction in heart failure. In the trial, fewer people who received the antibody targeting IL-1 were admitted to the hospital with heart failure compared to those who received the standard of care. The new findings may help to explain why.</p>
<p>Much more study is needed to determine if this treatment or others like it will prove beneficial for treating heart failure or other heart conditions that involve fibrosis. But these latest findings are a sign of encouraging progress in ongoing efforts to better understand and treat heart failure and potentially find ways to prevent or reverse damaging scars in the heart and other organs.</p>
<p><strong>Reference:</strong></p>
<p>Amrute JM, <em>et al</em>. <a href="https://pubmed.ncbi.nlm.nih.gov/39443792/" target="_blank" rel="noreferrer noopener">Targeting immune-fibroblast cell communication in heart failure</a>. <em>Nature</em>. DOI: 10.1038/s41586-024-08008-5 (2024).</p>
<p><em>NIH Support: National Heart, Lung, and Blood Institute; National Institute of Biomedical Imaging and Bioengineering; National Cancer Institute; National Institute of Arthritis and Musculoskeletal and Skin Diseases</em></p></p>
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<p><strong>Forwarded by:<br />
Michael Reeder LCPC<br />
Baltimore, MD</strong></p>
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