Review Article

Implication of Gut Microbiota in Cardiovascular Diseases

Table 2

Researches of gut microbiota in CVDs.

DiseasesSampleObservationsMechanismRef.

HypertensionHTN patientsDecreased butyrate-producing bacteria and butyrate levelSCFA-dependent[62]
Ang-II pretreated miceReduced BP after butyrate administration; increased zonulin levelSCFA-dependent; gut barrier dysfunction[65]
MiceIncreased BP after propionate treatmentOlfr78-dependent[66]
MiceDecreased BP after propionate treatmentGpr41-dependent[66]
Lactobacillus rhamnosus GG prevents HTN developmentReduced TMAO levels[70]
MiceHigh salt-induced HTNIncreased intestinal-derived corticosterone[72]
AtherosclerosisPatientsBacterial DNA observed in atherosclerotic plagues/[73]
Roseburia intestinalis ameliorates atherosclerosisAlter gene expression, induce fatty acid metabolism, and reduce inflammation response[77]
apoE-/- miceComparable atherosclerosis lesion in germ-free apoE-/- animals and their conventionally raised counterparts/[75]
Choline-enhanced atherosclerosis in aorta was off-set by antibioticsReduced macrophage and scavenger receptor CD36[76]
apoE-/- mice with HFDButyrate mitigates atherosclerotic plaque formationUpregulation of ABCA1 and subsequent cholesterol efflux[78]
Myocardial infarctionAMI rat modelIncreased Synergistetes phylum, Lachnospiraceae family, Spirochaetes phylum, Syntrophomonadaceae family, and Tissierella and Soehngenia generaIn parallel with gut barrier impairment[83]
STEMI patientsOver 12% plasma bacteria originated from the gutPartially associated with an inflammatory response[84]
Patients presenting with chest painPredictive value of plasma TMAO levels for incident cardiovascular eventsTMAO-related proinflammatory monocytes augment[85]
MiceImprove cardiac repair and post-MI outcome though modulation of immune compositionGut microbiota-derived SCFAs modulate immune composition[86]
Lactobacillus plantarum 299v improved ischemia tolerance and acute cardiac injury after MIReduce leptin level[87]
Heart failureMiceBacteroides fragilis reduces ventricular remodellingIncreased Foxp3+ Treg cells and anti-inflammatory cytokine[92]
Depletion of SCFAs finally leads to HFIntestinal barrier destruction, with endotoxin translocation[93, 94]
MiceTMAO alters cardiac muscle cells contractilityPromotion of calcium ions release[95, 96]
TMAO confers detrimental effects on adult cardiomyocytesT-tubule network damage; Ca handling dysfunction[97]
MicePulmonary edema, cardiac enlargement, and decreased ejection fractionTMAO-dependent[98]
PatientsTMAO increases susceptibility to HFInduction of myocardial fibrosis[99]
Overload-induced HF miceDMB ameliorates adverse cardiac structural remodellingDownregulating TMAO levels[100]
ArrhythmiaPatientsShared common features of gut microbiota dysbiosisAlike ratio of Firmicutes and Bacteroidetes[104, 105]
PatientsThrombus formation; platelet hyperreactivityElevated TMAO level[107]
TMAO stimulates ischemia-induced VARelease of proinflammatory markers such as IL-1β and TNF-α[109]
Canine AF modelGut microbes counteracts AF progressionTMAO production and CANS activation[110]
MiceReduced susceptibility to cardiac ventricular arrhythmiasSCFA-dependent[22]