"Scarring Complications from 'Creeping Fat' Occur in Crohn's Disease"
In a groundbreaking study, researchers have uncovered crucial insights into the role of a particular type of abnormal adipose tissue, known as 'creeping fat,' in the progression of Crohn's disease. This severe intestinal disease, which commonly begins in the teen or young adult years, can cause significant morbidity, with no approved anti-fibrotic therapies available to date.
The genetic pathways switched on in the creeping-fat fibroblasts suggest that these cells are primed to detect mechanical strain in the nearby intestine. This could be a significant finding, as the combination of inflammation in the intestine plus mechanical tension in intestinal tissue could drive the fibroblasts in nearby fat to participate in stricture formation. Strictures, which often form at the valve that joins the small intestine and the bowel, can affect up to 80% of those whose disease isn't put into remission by anti-inflammatories.
The researchers developed a mouse model that accurately replicates the biology of Crohn's disease, including strictures. They found that the activated fibroblasts in the interface between fat and bowel tissue clustered in a border region and were primed to manufacture more extracellular matrix, the fibrous substance that makes up scar tissue. The stiff, finger-like deposits of creeping fat that encase the intestines of Crohn's disease patients worsen the disease.
The team's work demonstrates that creeping fat-derived fibroblasts are important contributors to stricture progression in Crohn's disease. In an exciting development, they found that when the same experimental drug was used to interrupt YAP/TAZ signals in the fat cell fibroblasts in mice, the animals formed fewer strictures. This discovery helps explain why for many Crohn's patients, anti-inflammatories aren't sufficient to stop the disease.
The findings raise important questions about surgical management of intestinal strictures and suggest that future anti-fibrotic therapies will need to address both bowel and creeping fat-derived fibroblasts to achieve stricture remission. Patients with Crohn's disease often suffer from abdominal pain, diarrhea, malnutrition, weight loss, and fatigue. These new discoveries offer hope for a more comprehensive approach to managing this debilitating disease.
It's worth noting that fat-adipose tissue sends and receives hormonal, nervous system, and immune signals. The mechanism is surprisingly similar to the way scars form elsewhere, such as on the skin. However, more research is needed to fully understand the complex interplay between inflammation, mechanical strain, and fibroblast activation in the development and progression of Crohn's disease.
Unfortunately, there are no relevant search results available that provide information about the researchers involved in studying the effect of 'creeping fat' on Crohn's disease or the main publication of their research. As this field of study continues to evolve, we can expect to see further advancements in our understanding of Crohn's disease and potential new treatment options for patients.
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