Gut, Oral, and Fungal Microbiota in Hypertension: A Multi-Compartment Systematic Review.

The gut microbiota is an established modulator of blood pressure, but the oral bacteriome and the fungal mycobiome have been examined largely in isolation from it and from each other. No previous synthesis has evaluated all three compartments within one analytical framework, or treated sex and ethnicity as primary analytical axes rather than adjustment covariates. Systematic review reported according to PRISMA 2020 and, for the synthesis, the SWiM guideline. PubMed/MEDLINE, Embase, Scopus, and Web of Science were searched from inception to 30 June 2026. Observational human studies in adults reporting gut, oral, or fungal microbiota data stratified by blood pressure status were eligible, together with Mendelian randomisation studies and studies with a nested experimental causal component. Two reviewers screened and extracted independently, with a third resolving disagreement. Risk of bias was assessed with the Newcastle-Ottawa Scale and certainty of evidence with GRADE adapted for exposure-outcome questions. Increased abundance of the Ruminococcus gnavus group was the most convergent taxon-level finding, replicated in three independent populations on two continents, including one prospective multi-ethnic cohort with full adjustment and correction for multiple comparisons (OR 1.07, 95% CI 1.01-1.14 for incident hypertension). In the oral compartment, depletion of the nitrate-reducing commensal Neisseria subflava converged across a United States prospective cohort and an Italian case-control study using unrelated methods, and salivary nitric oxide was approximately three-fold lower in hypertensive subjects. Depletion of the short-chain fatty acid producers Faecalibacterium and Roseburia and enrichment of Klebsiella were convergent but geographically restricted. Mycobiome evidence was contradictory: two studies reported fungal dysbiosis, one of them already at the pre-hypertensive stage, while a cross-cohort metagenome-wide study on two independent cohorts from Beijing and Dalian (N = 159 hypertensive patients, 101 healthy controls) identified 61 gut bacterial species with consistent altered abundance across both cohorts while finding no replicable mycobiome signal. Recurring across compartments and kingdoms was the collapse of microbial co-correlation networks in hypertension, alongside a dissociation between null alpha diversity and significant beta diversity. Associations differed by ethnicity within a single multi-ethnic cohort and were generally stronger in women. Certainty of evidence, assessed per individual convergent finding, was very low for every taxon-level finding and low for salivary nitric oxide; these ratings concern the attribution of hypertension to specific organisms, not the existence of a microbiota-hypertension association, which is supported at community level in every compartment examined and by experimental transfer models. That the microbiota differs in hypertension is well supported; which organisms are responsible is not. The most reproducible signal is structural rather than taxonomic, and conventional differential-abundance analysis is not designed to detect it. No individual microbial taxon is currently ready to serve as a marker of hypertension or to inform clinical practice.