Gut microbiome as a novel cardiovascular therapeutic target

Abstract

Over the last two decades, our understanding of gut microbiotal composition and its association with intra- and extra-intestinal diseases including risk factors of cardiovascular disease (CVD) namely metabolic syndrome and atherosclerosis, have been increased exponentially. A pertinent question which often arises in researchers’ community is on how to manipulate the gut microbial ecology to ‘cure’ the cardiovascular risk factors. Accordingly, in this review we summarized the potential strategies, based on our current knowledge on gut microbiota in modulating CVD, how gut microbiota can be therapeutically exploited by targeting their metabolic activity to alleviate the risk factors of CVD.

The Gut Microbiome as Therapeutic Target in Central Nervous System Diseases: Implications for Stroke

“…These confounders might affect the composition of the intestinal microbial community as well [71]. Furthermore, as illustrated by the example of studies in atherosclerosis, microbiota may confer dualistic effects on the host—protective and harmful—in the pathogenesis and course of the disease [86] .…”

Human gut microbiota plays a role in the metabolism of drugs

“…changes in the structure and diversity of the microbiome are also associated with large array of pathological states such as inflammatory bowel diseases (iBds) (ref. 6 ), metabolic diseases such obesity and diabetes 7 , atherosclerosis 8 and cardiovascular disease 9 . The gut microbiome is relatively stable but its composition and/or function may be influenced by a range of factors such as diet 10 , probiotics 11 , and drugs, especially antibiotics 12 .…”

Gut Microbiome Derived Metabolites to Regulate Energy Homeostasis: How Microbiome Talks to Host

“…Several pathways have been proposed to be modulated by gut microbiome to cause metabolic syndrome, some of them are as follows; 1) gut microbiome helps to harvest extra energy from food that further increase extra energy accumulation in fat tissues, 2) gut microbiome mediated endotoxemia to create low grade inflammation and 3) production of certain detrimental metabolites that implicates dysregulation of several cellular function to aggravate disease progression [3,5]. For example, gut microbiome-derived TMAO induces cardiovascular diseases, acetate impairs insulin secretion and LPS escalates obesity and type 2 diabetes via increasing low grade inflammation [5][6][7]. To answer the question how microbiome interacts with host cells and impact metabolic function, later point explains the better link between gut microbiome and host in normal physiology.…”