Yusuke Sata1,2,3, Francine Z Marques4,5, David M Kaye6,7,8. 1. Human Neurotransmitters, Baker Heart and Diabetes Institute, 75 Commercial Road, Melbourne, Victoria, 3004, Australia. 2. Central Clinical School, Faculty of Medicine, Nursing and Health Sciences, Monash University, 99 Commercial Road, Melbourne, Victoria, 3004, Australia. 3. Department of Cardiology, Alfred Hospital, Philip Block, Level 3, 55 Commercial Road, Melbourne, Victoria, 3004, Australia. 4. Heart Failure Research Group, Baker Heart and Diabetes Institute, 75 Commercial Road, Melbourne, Victoria, 3004, Australia. 5. Hypertension Research Laboratory, School of Biological Sciences, Faculty of Science, Monash University, Wellington Road, Clayton, Victoria, 3800, Australia. 6. Central Clinical School, Faculty of Medicine, Nursing and Health Sciences, Monash University, 99 Commercial Road, Melbourne, Victoria, 3004, Australia. david.kaye@baker.edu.au. 7. Department of Cardiology, Alfred Hospital, Philip Block, Level 3, 55 Commercial Road, Melbourne, Victoria, 3004, Australia. david.kaye@baker.edu.au. 8. Heart Failure Research Group, Baker Heart and Diabetes Institute, 75 Commercial Road, Melbourne, Victoria, 3004, Australia. david.kaye@baker.edu.au.
Abstract
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. 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.
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. 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.
Entities:
Keywords:
Cardio-metabolic; Dysbiosis; Gut microbiome; Gut microbiota; Heart failure; Hypertension; Metabolites
Authors: Xingxing Li; Zongjing Fan; Jie Cui; Dong Li; Jinjin Lu; Xiaoyun Cui; Liandi Xie; Yang Wu; Qian Lin; Yan Li Journal: Front Cardiovasc Med Date: 2022-02-16