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Abstract of the day - Inflammatory bowel disease and increased CVD – what is the mechanism?

27 Aug 2023
Abstract of the Day

Several studies have linked inflammatory bowel disease (IBD) with the development of CVD;1 however, the molecular mechanisms by which IBD impairs the CV system have not been fully elucidated. Today, Associate Professor Qingjie Li (University of Texas Medical Branch - Galveston, USA) describes a study exploring whether dysbiosis plays a role in gut-heart crosstalk.

Cardiac impairment was investigated in three preclinical models: dextran sodium sulphate (DSS)-induced colitis in mice, trinitrobenzenesulfonic acid-induced colitis in rats and IL-10-deficient mice that develop spontaneous colitis. In all three models, decreased LVEF, increased LV mass and elevated serum B-type natriuretic peptide was observed, providing direct evidence that chronic colitis deteriorates the heart. Furthermore, RNA sequencing revealed loss of brain-derived neurotrophic factor (Bdnf) expression and alterations in multiple genes critical to myocardial homeostasis. More recently, the authors found that several commonly dysregulated cardiac genes were significantly rescued by faecal microbiota transplanted from wild-type mice. Many of the colitis-induced changes, including Bdnf reduction, were also observed in microbiota-depleted C57BL/6J mice and germ-free mice receiving dysbiotic faecal microbiome, suggesting that dysbiosis impaired the heart by suppressing Bdnf. Indeed, cardiac-­specific Bdnf knockout mice displayed impaired cardiac function, including decreased contractility and ejection fraction, increased fibrosis and diminished coronary microcirculation as compared to wild-type mice.

The researchers then found that miR­-155 in the heart and exosomal miR­-29b in the plasma were significantly elevated by chronic colitis, and interestingly, miR-­155 and miR-­29b mimics suppressed BDNF in cardiomyocytes both in vitro and in vivo. Of note, miR-­155 inhibitors or exosomes packaged with miR-­29b antagonists ameliorated the Bdnf reduction seen in the hearts of IL-10-deficient mice, while BDNF supplementation markedly improved heart function in DSS mice.

The authors concluded that targeting the dysbiosis/miR-29b/miR-155/BDNF signalling axis may be a promising approach to overcome colitis-induced cardiac impairment. Next steps may include verifying the therapeutic efficacy of BDNF supplementation in IL-10-deficient mice, confirming the detrimental effect of dysbiotic microbiota by transplanting faecal microbiota of IBD patients or healthy control subjects into germ-free mice, and elucidating the molecular mechanisms by which IBD induces cardiac fibrosis.


  1. Xiao Y, et al. Am J Physiol Regul Integr Comp Physiol. 2023;325:R193–R211.