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Hypoxia is a key mechanism for regulating inflammation in ulcerative colitis

Russian Open Medical Journal 2020 5 citations ? Citation count from OpenAlex, updated daily. May differ slightly from the publisher's own count. Score: 30 ? 0–100 AI score estimating relevance to the microplastics field. Papers below 30 are filtered from public browse.
Ekaterina Postovalova, О. В. Макарова, А. М. Косырева, D. Sh. Dzhalilova

Summary

This review examines how tissue hypoxia regulates inflammation in ulcerative colitis, a chronic bowel disease. While not directly about microplastics, it is relevant because microplastic exposure has been associated with gut inflammation and disruption of the intestinal barrier in emerging research.

Intestinal bowel diseases (IBD), including ulcerative colitis (UC), is the group of difficult to diagnose widespread among the population diseases. Pathogenesis of the disease is associated with a complex interaction of the genetic factors, the environment, the microbiome and the unpredicted reaction of the immune system, and the existing treatment methods are not effective enough. It is known, that hypoxia plays a key role in both system and local inflammatory reactions, mainly due to microcirculatory disorders and disseminated intravascular coagulation. Therefore a lot of studies have demonstrated that severity of any inflammatory diseases, including Crohn's disease (CD) and UC depends on hypoxia resistance. In this review we discussed microcirculation of blood and physiological hypoxia in the intestine, the role of hypoxia-inducible factors in the development of IBD and UC, as well as their influence on the severity of the inflammatory process. Authors described the protective effect of various PHD inhibitors and its benefits and disadvantages, so as new approaches of searching of very specific low molecular weight substanses as drugs for the control of IBD and UC.

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