From Microbes to Myocardium: A Comprehensive Review of the Impact of the Gut-Brain Axis on Cardiovascular Disease. Cureus Cardiovascular diseases (CVDs) remain the leading cause of morbidity and mortality worldwide despite advances in medical research and therapeutics. Emerging evidence suggests a significant role of the gut-brain axis, a complex communication network involving the gut microbiota, central nervous system, and cardiovascular system, in modulating cardiovascular health. The gut microbiota influences systemic inflammation, neurohumoral pathways, and metabolic processes, which are critical in the pathogenesis of CVD. Dysbiosis, or an imbalance in the gut microbiota, has been implicated in various cardiovascular conditions, including hypertension, atherosclerosis, and heart failure. This comprehensive review aims to elucidate the intricate relationship between the gut microbiome, brain, and cardiovascular system, highlighting the mechanisms by which gut-derived signals affect cardiovascular function. Key microbial metabolites, such as short-chain fatty acids (SCFAs) and trimethylamine N-oxide (TMAO), and their impact on vascular health and blood pressure regulation are discussed. Furthermore, the review explores potential therapeutic strategies targeting the gut-brain axis, including probiotics, prebiotics, dietary modifications, and pharmacological interventions, to improve cardiovascular outcomes. Despite promising findings, the field faces challenges such as individual variability in microbiome composition, complexities in gut-brain interactions, and the need for robust clinical trials to establish causality. Addressing these challenges through interdisciplinary research could pave the way for innovative, personalized therapeutic approaches. This review provides a comprehensive understanding of the gut-brain-cardiovascular axis, underscoring its potential as a novel target for preventing and treating CVD. 10.7759/cureus.70877

Gut commensal Parabacteroides distasonis exerts neuroprotective effects in acute ischemic stroke with hyperuricemia via regulating gut microbiota-gut-brain axis. Journal of translational medicine BACKGROUND:Hyperuricemia is considered as an independent risk factor for acute ischemic stroke (AIS), and some AIS patients are accompanied by an increase in serum uric acid. Recent studies have highlighted the important role of gut microbiota in both hyperuricemia and AIS, but there is little available data on the relationship between gut microbiota and the pathogenesis of AIS with hyperuricemia (HAS). METHODS:Here we profiled the gut microbiota composition in 63 HAS patients and 269 non-HAS patients through 16s rRNA sequencing. Male rat with hyperuricemia were subjected to middle cerebral artery occlusion (MCAO) to establish HAS model and were then treated with Parabacteroides distasonis. Subsequently, the neurological deficit, pathological damages and blood-brain barrier disruption were evaluated. Moreover, the levels of ROS, inflammatory cytokines, NF-𝜿B pathway related protein, and vascular density markers were determined. RESULTS:There were significant differences of gut microbiota composition between HAS patients and non-HAS patients, and a significant decrease in the abundance of Parabacteroides in HAS patients compared to non-HAS patients. Animal experiments showed that supplementation with P. distasonis increased beneficial commensal bacteria, significantly improved neurological deficits, pathological damages and BBB disruption, as well as reduced the level of serum uric acid in HAS rats. We further demonstrated that P. distasonis treatment decreased ROS level and increased SOD2 level, thereby reducing oxidative stress. Meanwhile, P. distasonis effectively inhibited NF-𝜿B signal pathway and reduced the production of inflammatory cytokines, including TNF-α and IL-1β, alleviating the inflammatory response. Notably, P. distasonis treatment increased the levels of vascular density markers including cluster of differentiation 31 (CD31) and alpha-smooth muscle actin (α-SMA), ameliorating vascular damage in HAS rats. CONCLUSIONS:Together, these findings highlighted the important role of P. distasonis in the pathogenesis of HAS, and its mechanism was involved in the regulation of gut microbiota-gut-brain axis, which implied a novel strategy against HAS. 10.1186/s12967-024-05800-9