Editorial
Copyright ©The Author(s) 2025.
World J Gastroenterol. Jan 7, 2025; 31(1): 102042
Published online Jan 7, 2025. doi: 10.3748/wjg.v31.i1.102042
Table 1 Mechanisms involved in the formation and maintenance of creeping fat in Crohn’s disease
Mechanism
Description
Ref.
Bacterial translocationMigration of bacteria from the intestinal lumen to the mesenteric adipose tissue, stimulating local inflammationHa et al[22]
Chronic inflammationContinuous production of inflammatory cytokines (such as tumor necrosis factor-α, interleukin-6, and interleukin-1β) that affect the mesenteryWu et al[14]; Foppa et al[24]
Local adipokine productionRelease of leptin and adiponectin from adipose tissue, which modulates the immune and inflammatory responsesTsounis et al[19]
Hypoxia and local fibrosisThe expansion of mesenteric fat can generate hypoxia, favoring fibrosis and aggravating the inflammatory conditionWu et al[14]; Li et al[33]
Alteration of gut microbiotaChanges in the composition of the intestinal microbiota that affect the metabolism and function of the adipose tissueGilliland et al[4]; Ha et al[22]
Activation of macrophages and T cellsInfiltration of macrophages and T cells into adipose tissue, perpetuating inflammation and tissue remodelingKaraskova et al[12]; Tsounis et al[19]