|
Diseases | Sample | Observations | Mechanism | Ref. |
|
Hypertension | HTN patients | Decreased butyrate-producing bacteria and butyrate level | SCFA-dependent | [62] |
Ang-II pretreated mice | Reduced BP after butyrate administration; increased zonulin level | SCFA-dependent; gut barrier dysfunction | [65] |
Mice | Increased BP after propionate treatment | Olfr78-dependent | [66] |
Mice | Decreased BP after propionate treatment | Gpr41-dependent | [66] |
| Lactobacillus rhamnosus GG prevents HTN development | Reduced TMAO levels | [70] |
Mice | High salt-induced HTN | Increased intestinal-derived corticosterone | [72] |
Atherosclerosis | Patients | Bacterial DNA observed in atherosclerotic plagues | / | [73] |
| Roseburia intestinalis ameliorates atherosclerosis | Alter gene expression, induce fatty acid metabolism, and reduce inflammation response | [77] |
apoE-/- mice | Comparable atherosclerosis lesion in germ-free apoE-/- animals and their conventionally raised counterparts | / | [75] |
| Choline-enhanced atherosclerosis in aorta was off-set by antibiotics | Reduced macrophage and scavenger receptor CD36 | [76] |
apoE-/- mice with HFD | Butyrate mitigates atherosclerotic plaque formation | Upregulation of ABCA1 and subsequent cholesterol efflux | [78] |
Myocardial infarction | AMI rat model | Increased Synergistetes phylum, Lachnospiraceae family, Spirochaetes phylum, Syntrophomonadaceae family, and Tissierella and Soehngenia genera | In parallel with gut barrier impairment | [83] |
STEMI patients | Over 12% plasma bacteria originated from the gut | Partially associated with an inflammatory response | [84] |
Patients presenting with chest pain | Predictive value of plasma TMAO levels for incident cardiovascular events | TMAO-related proinflammatory monocytes augment | [85] |
Mice | Improve cardiac repair and post-MI outcome though modulation of immune composition | Gut microbiota-derived SCFAs modulate immune composition | [86] |
| Lactobacillus plantarum 299v improved ischemia tolerance and acute cardiac injury after MI | Reduce leptin level | [87] |
Heart failure | Mice | Bacteroides fragilis reduces ventricular remodelling | Increased Foxp3+ Treg cells and anti-inflammatory cytokine | [92] |
| Depletion of SCFAs finally leads to HF | Intestinal barrier destruction, with endotoxin translocation | [93, 94] |
Mice | TMAO alters cardiac muscle cells contractility | Promotion of calcium ions release | [95, 96] |
| TMAO confers detrimental effects on adult cardiomyocytes | T-tubule network damage; Ca handling dysfunction | [97] |
Mice | Pulmonary edema, cardiac enlargement, and decreased ejection fraction | TMAO-dependent | [98] |
Patients | TMAO increases susceptibility to HF | Induction of myocardial fibrosis | [99] |
Overload-induced HF mice | DMB ameliorates adverse cardiac structural remodelling | Downregulating TMAO levels | [100] |
Arrhythmia | Patients | Shared common features of gut microbiota dysbiosis | Alike ratio of Firmicutes and Bacteroidetes | [104, 105] |
Patients | Thrombus formation; platelet hyperreactivity | Elevated TMAO level | [107] |
| TMAO stimulates ischemia-induced VA | Release of proinflammatory markers such as IL-1β and TNF-α | [109] |
Canine AF model | Gut microbes counteracts AF progression | TMAO production and CANS activation | [110] |
Mice | Reduced susceptibility to cardiac ventricular arrhythmias | SCFA-dependent | [22] |
|