Table 1.
The association between gut microbiota and the development and progression of CVD.
| Hypertension | Atherosclerosis | Heart failure | |
|---|---|---|---|
| Participation of gut microbiota | α diversity↓, Prevotella↑, the F/B ratios↑, Erwinia↑, Corynebacteriac‐eae↑, Anaerostipes↓, Lactobacillus murinus↓ | Streptococcus↑, Enterobacteriaceae↑, Lactobacillales↑, Clostridium subcluster XIVa↑, Bacteroides↓ | Campylobacter↑, Candida↑, Shigella↑, Salmonella↑, Yersinia enterocolitica↑, Escherichia/Shigella↑ |
| Participation of gut microbial metabolites |
SCFAs 4‐ethylphenylsulfate |
TMAO↑ BAs, butyrate, NAPEs |
TMAO↑ Plasma primary BAs↓, specific secondary BAs↑ Propionate, PAG, PCS |
| Summary of potential mechanisms | GPCRs (GPR42, Olfr78 and Gper1) related signalling to elicit biological effects |
Intestinal permeability↑ Endothelial cell–cell conjunctions↓ and cell permeability↑ TLR activation↑ Macrophage scavenger receptors and CD36↑ NF‐κB and inflammasome activation↑ Cyp7a1 and Cyp27a1↓ Intracellular Ca2+ release↑ |
Intestinal perfusion↓ and congestion↑ Intestinal permeability↑ Prolong the effect of angiotensin↑ NLRP3 inflammasome‐associated TGF‐β/Smad3 signalling activation↑ |
| Medications |
Captopril: Allobaculum↑ Candesartan and Irbesartan: normalize the F/B ratio, preserve Lactobacillus levels |
Statins: Firmicutes↓, Proteobacteria↑, BAs alteration, butyrate↓ Aspirin:Prevotella, Bacteroides, Ruminococcaceae and Barnesiella alterations, TMAO‐mediated platelet hyper‐responsiveness↓ |
Digoxin: Eggerthella lenta could inactivate digoxin |