๐ก The global surge in age-related cardiovascular diseases has prompted extensive research into novel therapeutic avenues. This review delves into the intricate relationship between gut microbiota composition and age-related cardiovascular diseases, emphasizing key metabolites like trimethylamine N-oxide (TMAO), bile acids (BAs), and short-chain fatty acids (SCFAs). The study explores molecular pathways affected by gut microbiota dysbiosis and suggests the gut microbiota as a promising therapeutic target for mitigating cardiovascular diseases.
๐ Atherosclerosis:
Atherosclerotic plaques harbor diverse bacterial DNA, indicating a microbial environment.
Patients with atherosclerotic cardiovascular disease exhibit altered gut microbiota, particularly higher levels of ๐๐ต๐ณ๐ฆ๐ฑ๐ต๐ฐ๐ค๐ฐ๐ค๐ค๐ถ๐ด ๐ข๐ฏ๐ฅ ๐๐ฏ๐ต๐ฆ๐ณ๐ฐ๐ฃ๐ข๐ค๐ต๐ฆ๐ณ๐ช๐ข๐ค๐ฆ๐ข๐ฆ.
Gut microbiota dysbiosis contributes to atherosclerosis development through oxidative stress and inflammation.
Microbial metabolites like TMAO promote atherosclerosis by inducing endothelial dysfunction and inflammation.
๐ Hypertension:
Gut-brain axis dysfunction is implicated in hypertension, involving bidirectional communication between gut microbiota and the brain.
Neuroinflammation triggered by gut-brain axis dysfunction elevates inflammatory mediators, impacting blood pressure regulation.
Long-term high-salt diets increase TMAO levels, promoting neuroinflammation and oxidative stress, contributing to hypertension.
๐ Myocardial Infarction and Heart Failure:
Patients with myocardial infarction and heart failure experience increased intestinal permeability and bloodstream infections.
๐๐ข๐ค๐ต๐ฐ๐ฃ๐ข๐ค๐ช๐ญ๐ญ๐ถ๐ด, ๐๐ข๐ค๐ต๐ฆ๐ณ๐ฐ๐ช๐ฅ๐ฆ๐ด, ๐ข๐ฏ๐ฅ ๐๐ต๐ณ๐ฆ๐ฑ๐ต๐ฐ๐ค๐ฐ๐ค๐ค๐ถ๐ด from the gut are detected in blood microbiomes of patients with myocardial infarction.
Intestinal bacteria and LPS in systemic circulation trigger monocyte recruitment, systemic inflammation, and cardiovascular events.
SCFAs, particularly butyrate, contribute to cardiac repair and improved prognosis after myocardial infarction.
๐ Myocardial Hypertrophy and Fibrosis:
Probiotics, prebiotics, and biotin administration improves gut microbiota composition, reducing cardiac hypertrophy induced by hypobaric hypoxia.
LPS induces cardiac oxidative stress, myocardial and perivascular fibrosis, linking gut microbiota to pathological cardiac remodeling.
Elevated TMAO levels are associated with heart failure, left ventricular dysfunction, and increased susceptibility to ventricular arrhythmias.
๐ Arrhythmia:
๐๐ข๐ฆ๐ค๐ข๐ญ๐ช๐ฃ๐ข๐ค๐ต๐ฆ๐ณ๐ช๐ถ๐ฎ ๐ข๐ฏ๐ฅ ๐๐ด๐ค๐ช๐ญ๐ญ๐ช๐ฃ๐ข๐ค๐ต๐ฆ๐ณ abundance decreases in patients with atrial fibrillation, while ๐๐ถ๐ฎ๐ช๐ฏ๐ฐ๐ค๐ฐ๐ค๐ค๐ถ๐ด, ๐๐ต๐ณ๐ฆ๐ฑ๐ต๐ฐ๐ค๐ฐ๐ค๐ค๐ถ๐ด, ๐ข๐ฏ๐ฅ ๐๐ฏ๐ต๐ฆ๐ณ๐ฐ๐ค๐ฐ๐ค๐ค๐ถ๐ด increase.
SCFAs attenuate NLRP3 inflammasome activation, reducing the occurrence of atrial fibrillation.
High TMAO levels promote atrial fibrillation by inducing left atrial inflammation and fibrosis.
PAGln, a gut microbiota-derived metabolite, increases oxidative stress and atrial cell apoptosis, promoting atrial fibrillation.
๐ Gut Microbiome as a Potential Therapeutic Direction:
Fecal microbiota transplantation (FMT) shows promise in restoring microbial balance and improving insulin sensitivity in patients with cardiometabolic syndrome.
Specific inhibition of FXR in the intestine could reduce TMAO production without affecting cholesterol metabolism.
Maintaining a healthy gut flora through dietary optimization, prebiotics, and probiotics emerges as crucial for cardiovascular health.
Link to the article : http://tinyurl.com/yc8z2yhj
