Table 1.
Studies to control intestinal gut metabolites useful in endothelial dysfunction related cardiovascular diseases.
Disorder | Model | Metabolite(s) | Intervention | Prevalent Mechanism | Reference |
---|---|---|---|---|---|
Coronary artery disease | Mouse cells and tissue | TMAO | DMB | Inhibition of foam cell formation | [56] |
FMO3 silencing or inhibition | [78] | ||||
Resveratrol | [63] | ||||
Mouse tissue | - | Probiotics | Reduce vascular inflammation | [79] | |
Hypertension | Mouse | SCFA | SCFA | Activation of G-protein coupled receptor-41 | [45,80] |
Mouse tissue | SCFA | High-fiber diet | Increased SCFA-producing bacteria | [81,82,83,84,85,86] | |
Human hypertensive patients | - | Dietary fibers, probiotics | Regulation of renin–angiotensin system. | [86,87,88,89,90] | |
Human hypertensive patients | - | Minocycline, Vancomycin | Increased the diversity of GM and reduced Firmicutes | [36,91] | |
Hypertension and endothelial dysfunction | Spontaneous hypertensive rats (SHR) | - | Gallic acid | Angiotensin converting enzyme inhibition | [92] |
Endothelial dysfunction | Cultured cells | Uremic toxins | Caffeic acid | Increased NO production and reduced ROS | [76] |