TY - JOUR
T1 - The Emerging Role of Gut Dysbiosis in Cardio-metabolic Risk Factors for Heart Failure
AU - Sata, Yusuke
AU - Marques, Francine Z.
AU - Kaye, David M.
PY - 2020/5/1
Y1 - 2020/5/1
N2 - Purpose of Review: To summarize the recent evidence that supports a role for the gut microbiota, microbiota-derived metabolites, and dysbiosis on cardiovascular risk factors, and to discuss the neuro-cardio-metabolic mechanisms that link gut microbiota and heart failure. Recent Findings: There is growing evidence that the gut microbiota communicates with and impacts the cardiovascular system, contributing to the development of heart failure once it becomes out of balance (i.e. gut dysbiosis). The exact mechanisms of how the gut microbiota influences cardiovascular outcomes are not fully understood, but immune dysregulation and disturbance of neuro-enteroendocrine hormones seem to be involved. The disturbances in the gut microbiota influence the progression of several risk factors for heart failure, including atherosclerosis, obesity, diabetes, kidney disease and hypertension. In turn, these conditions also act to regulate the gut microbiota through the deterioration of the integrity of the intestinal barrier and the release of neurotransmitters and gastrointestinal hormones. In normal and healthy physiological conditions, these interactions are homeostatic and tightly controlled. However, a combination of environmental exposures (e.g. antibiotics use and Western diet) and the host’s intrinsic conditions (e.g. genetics and fluid status) can result in the breakdown of intestinal homeostasis and further progression of cardiovascular risk factors, which lead to the development of heart failure. Summary: Manipulation of the gut microbiota may have the potential to improve cardiovascular outcomes by ameliorating immune system dysregulation, enteroendocrine disruptions, and neurohormonal activation in patients with cardiovascular risk factors for heart failure.
AB - Purpose of Review: To summarize the recent evidence that supports a role for the gut microbiota, microbiota-derived metabolites, and dysbiosis on cardiovascular risk factors, and to discuss the neuro-cardio-metabolic mechanisms that link gut microbiota and heart failure. Recent Findings: There is growing evidence that the gut microbiota communicates with and impacts the cardiovascular system, contributing to the development of heart failure once it becomes out of balance (i.e. gut dysbiosis). The exact mechanisms of how the gut microbiota influences cardiovascular outcomes are not fully understood, but immune dysregulation and disturbance of neuro-enteroendocrine hormones seem to be involved. The disturbances in the gut microbiota influence the progression of several risk factors for heart failure, including atherosclerosis, obesity, diabetes, kidney disease and hypertension. In turn, these conditions also act to regulate the gut microbiota through the deterioration of the integrity of the intestinal barrier and the release of neurotransmitters and gastrointestinal hormones. In normal and healthy physiological conditions, these interactions are homeostatic and tightly controlled. However, a combination of environmental exposures (e.g. antibiotics use and Western diet) and the host’s intrinsic conditions (e.g. genetics and fluid status) can result in the breakdown of intestinal homeostasis and further progression of cardiovascular risk factors, which lead to the development of heart failure. Summary: Manipulation of the gut microbiota may have the potential to improve cardiovascular outcomes by ameliorating immune system dysregulation, enteroendocrine disruptions, and neurohormonal activation in patients with cardiovascular risk factors for heart failure.
KW - Cardio-metabolic
KW - Dysbiosis
KW - Gut microbiome
KW - Gut microbiota
KW - Heart failure
KW - Hypertension
KW - Metabolites
UR - http://www.scopus.com/inward/record.url?scp=85084263624&partnerID=8YFLogxK
U2 - 10.1007/s11906-020-01046-0
DO - 10.1007/s11906-020-01046-0
M3 - Review Article
C2 - 32385705
AN - SCOPUS:85084263624
VL - 22
JO - Current Hypertension Reports
JF - Current Hypertension Reports
SN - 1522-6417
IS - 5
M1 - 38
ER -