Gut microbiota dysbiosis, chronic inflammation and atherosclerosis: a review of cellular mechanisms and host-microbe interactions
A narrative review maps the pathways through which gut dysbiosis sustains vascular inflammation and atherosclerosis progression.
Context
Atherosclerosis is the leading cause of cardiovascular mortality worldwide. Identifying modifiable upstream contributors such as gut microbiota composition justifies mechanistic investigation.
What the study showed
The abstract describes three interconnected processes: metabolite imbalance (reduced SCFAs, elevated TMAO and LPS), intestinal barrier dysfunction with microbial translocation, and systemic immune reprogramming. Clinical studies link gut-derived biomarkers—particularly TMAO and LPS-related signals—to atherosclerotic burden and adverse cardiovascular outcomes. Experimental models using fecal microbiota transplantation, probiotics, antibiotics, and gene-deficient animals support a contributory role of the gut-immune-vascular axis.
How it was done
Narrative review without formal meta-analysis. No participant n is defined; the abstract does not specify a systematic search protocol or explicit inclusion criteria.
Limitations
Analysis is based solely on the abstract without access to the full text. The abstract itself acknowledges cross-study heterogeneity and limited causal evidence in humans; narrative reviews are susceptible to selection bias.
In clinical practice
No direct clinical recommendation is supported by this study. The microbiota-atherosclerosis relationship remains biologically plausible but requires controlled clinical trials to establish causality and intervention efficacy.