This process is known as the granulation phase and is critical for healing. But due to bodily response in the form of inflammation and scarring, this phase simultaneously reduces cardiac function, significantly increasing the risk of future cardiac events, including heart failure.
Now, a new study published by Vanderbilt mechanobiology researchers details a possible solution for fine-tuning inflammation and cellular activity in cardiac recovery -- thanks to an antibody initially developed for rheumatoid arthritis.
Paper - Today - Journal - JCI - Insight
The paper is available today in the journal JCI Insight.
The research, conducted by a collaborative team from the Merryman Mechanobiology Laboratory at Vanderbilt University and medical research labs at Vanderbilt University Medical Center, looks at the inflammation phase after myocardial infarction events and is the first to target a specific protein, known as cadherin-11 -- a major contributor to inflammation in cardiac fibrosis.
Findings - Work - Cadherin-11 - Paper - Vanderbilt
The new findings are significant as they build on existing work looking at cadherin-11, including a 2017 paper from the Vanderbilt team which showed how this particular antibody could target cadherin-11 to prevent calcific aortic valve disease.
"Some amount of inflammation is necessary in myocardial infarction, but becomes excessive and causes adverse side effects," noted senior author W. David Merryman, Walters Family Chair in the School of Engineering and a Professor of Biomedical Engineering, Pharmacology, Medicine, and Pediatrics. "This latest work with the antibody shows...
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The beatings will continue until moral improves.