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The role of diet-derived short-chain fatty acids in regulating cardiac pressure overload
Nikolai Pakhomov1, John A Baugh1
1UCD Conway Institute for Biomolecular and Biomedical Research, School of Medicine, University College Dublin, Dublin, Ireland.
Insights
Dietary fiber intake promotes gut bacteria that produce short-chain fatty acids (SCFAs). These SCFAs may help manage hypertension and heart failure with preserved ejection fraction (HFpEF) by modulating immune responses and cardiac pathology.
Area of Science:
- Cardiovascular Medicine
- Gastroenterology
- Microbiology
Background:
- Heart failure (HF), particularly HF with preserved ejection fraction (HFpEF), is a growing global health concern.
- Hypertension-induced pressure overload is a primary driver of cardiac hypertrophy, fibrosis, and diastolic dysfunction, leading to HFpEF.
- Current treatments for established HFpEF are limited, highlighting the need for novel therapeutic strategies targeting underlying inflammatory and fibrotic processes.
Purpose of the Study:
- To explore the potential therapeutic role of short-chain fatty acids (SCFAs) in managing hypertension and associated cardiac damage.
- To review the mechanisms by which SCFAs, derived from gut microbiota fermentation of dietary fiber, may influence cardiovascular health.
- To emphasize the link between gut microbiota, dietary fiber, and SCFA production in mitigating pressure overload-induced cardiac pathology.
Main Methods:
- Literature review focusing on the interplay between gut microbiota, dietary fiber, SCFAs, and cardiovascular disease.
- Analysis of studies investigating the effects of SCFAs on blood pressure regulation and immune modulation.
- Examination of research on SCFA mechanisms in cardiac responses to pressure overload and fibrosis.
Main Results:
- High-fiber diets are associated with protective effects against systemic hypertension and cardiac pathology.
- Gut microbiota-derived SCFAs play a crucial role in mediating these protective effects.
- Emerging evidence suggests SCFAs can modulate immune responses and systemic circulation, offering potential therapeutic benefits.
Conclusions:
- Dietary soluble fiber and SCFA-producing bacteria represent a promising avenue for managing hypertension and preventing HFpEF.
- Targeting the gut microbiota and SCFA production could offer novel strategies to halt or reverse cardiac damage caused by pressure overload.
- Further research into SCFA-mediated mechanisms is warranted to develop effective interventions for cardiovascular diseases.
Abstract:
Heart failure (HF) is one of the leading causes of mortality and morbidity in the modern world whose increasing prevalence is associated with "Western" diet and sedentary lifestyles. Of particular concern is the increasing burden of HF with preserved ejection fraction (HFpEF) that involves complex pathophysiology and is difficult to treat. Pressure overload caused by hypertension (HTN) is the predominant driver of cardiac injury, left ventricular hypertrophy, and fibrosis that progresses to diastolic dysfunction and ultimately HFpEF. Although pharmacological control of blood pressure may affect the degree of pressure overload, such therapies are largely ineffective in established HFpEF, and there is a need to modulate the festering inflammatory and fibrotic response to injury to halt and perhaps reverse pathology. An emerging literature indicates potentially important links between the gut microbiota, dietary soluble fiber, and microbiota-derived metabolites that modulate blood pressure and the immune response. In particular, high-fiber diets demonstrate protective properties in systemic hypertension and left-sided cardiac pathology, and this action is closely associated with short-chain fatty acid (SCFA)-producing bacteria. Mechanisms underlying the beneficial action of SCFAs in immunity and the systemic circulation could potentially be applied to the treatment of hypertension and the cardiac damage it causes. In this review, we discuss the potential beneficial effects of SCFAs, with an emphasis on mechanisms that are involved in cardiac responses to pressure overload.
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