COMMON THERAPEUTIC TARGETS OF ATHEROSCLEROSIS AND CROHN DISEASE: A NARRATIVE REVIEW

Authors

  • Alexander V. Blagov Author
  • Marina D. Sazonova Author
  • Mikhail A. Popov Author
  • Alexander N. Orekhov Author
  • Vasily P. Karagodin Author
  • Margarita A. Sazonova Author
  • Yuri V. Arkhipenko Author
  • Andrey V. Omelchenko Author

DOI:

https://doi.org/10.4238/seg03a57

Keywords:

Atherosclerosis; Crohn disease; Inflammation; Therapeutic targets; Cytokines; Gut microbiota

Abstract

Atherosclerosis and Crohn disease have long been regarded as unrelated disorders, yet a growing body of epidemiological and mechanistic evidence places them on a shared inflammatory continuum. Patients with inflammatory bowel disease, and Crohn disease in particular, carry an independent excess risk of ischemic heart disease and myocardial infarction that is most pronounced during periods of active intestinal inflammation. Both conditions are chronic, immune-mediated diseases in which an aberrant interaction between innate and adaptive immunity, the vascular or mucosal endothelium, lipid handling, and the gut microbiota perpetuates tissue injury. This narrative review synthesizes the molecular and cellular targets that the two diseases hold in common and the therapeutic developments that have grown out of them. The targets discussed include tumor necrosis factor-alpha, the interleukin-12 and interleukin-23 to T-helper-17 axis, the interleukin-1-beta and NLRP3 inflammasome pathway, interleukin-6 signaling, the Janus kinase and signal transducer and activator of transcription cascade, leukocyte adhesion and trafficking molecules, endothelial dysfunction with oxidative stress, and the gut microbiota and its metabolite trimethylamine N-oxide. We show how agents engineered for one disease inform or directly treat the other: anti-tumor-necrosis-factor and anti-interleukin-12 and 23 biologics control intestinal inflammation and may favorably influence vascular risk, while interleukin-1-beta blockade and low-dose colchicine reduce cardiovascular events by dampening the same inflammasome pathway that drives intestinal disease. We also highlight where target biology diverges and where safety signals demand caution. Two summary tables compare the shared targets and catalogue the corresponding therapeutic developments. A common-target framework supports rational drug repurposing, biomarker-guided therapy, and integrated cardiovascular and gastrointestinal risk management, but dedicated outcome trials in inflammatory bowel disease populations remain necessary to confirm cross-disease benefit.

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Published

2026-06-25

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Section

Articles