Comorbidity Mechanism Between Ulcerative Colitis and Atrial Fibrillation Based on "Gut Microbiota-gut-heart" Axis
10.13422/j.cnki.syfjx.20251440
- VernacularTitle:基于“肠道菌群-肠-心轴”探讨溃疡性结肠炎与心房颤动的共病机制
- Author:
Meiyu FENG
1
;
Wenjing ZHANG
2
;
Yihang DU
2
;
Xuanye DING
1
;
Yuanhui HU
2
;
Haitai YUAN
3
Author Information
1. Shandong First Medical University， Jinan 250117， China
2. Guang'anmen Hospital， China Academy of Chinese Medical Sciences， Beijing 100053， China
3. Shandong Provincial Hospital， Jinan 250021， China
- Publication Type:Journal Article
- Keywords:
gut microbiota;
gut microbiota metabolites;
atrial fibrillation;
ulcerative colitis;
fecal microbiota transplantation
- From:
Chinese Journal of Experimental Traditional Medical Formulae
2026;32(7):276-281
- CountryChina
- Language:Chinese
-
Abstract:
The gut microbiota is regarded as the "eighth organ" of the human body and plays a critical regulatory role in the occurrence and progression of various diseases. Ulcerative colitis （UC） is a chronic inflammatory bowel disease with a complex etiology and a tendency toward recurrent episodes. In recent years， studies have shown that gut microbiota dysbiosis plays a key role in its pathological processes. Meanwhile， an increasing number of studies have demonstrated that imbalances in the gut microbiota and abnormalities in its metabolites are closely associated with the development of atrial fibrillation （AF）. Although UC and AF belong to diseases of the digestive system and cardiovascular system， respectively， both exhibit systemic inflammatory characteristics and are often accompanied by gut microbiota dysregulation and abnormal metabolic products. However， systematic investigations into the mechanisms by which gut microbiota-derived metabolites act in these two diseases remain limited. Based on this， the present study adopts literature review and theoretical analysis methods， taking the "gut microbiota-gut-heart" axis as the entry point， to systematically summarize the signaling networks of three key classes of metabolites， i.e.， short-chain fatty acids （SCFAs）， bile acids （BAs）， and trimethylamine N-oxide （TMAO）， in the comorbidity mechanism of UC and AF. The findings indicate that these metabolites may activate key inflammatory pathways， such as NF-κB and NLRP3， thereby synergistically mediating intestinal barrier dysfunction and systemic inflammation and constructing a potential comorbidity network. On this basis， potential intervention strategies for the treatment of UC-AF comorbidity， including probiotic intervention and fecal microbiota transplantation， are further discussed. This study aims to provide new theoretical evidence and research perspectives for prevention and treatment strategies of cross-system diseases.
