Why the study?
Clinical trials targeting immune effectors in HF have consistently failed, prompting attention to how the gut microbiota modulates immune mechanisms and cardiac remodelling.
Does modulation of the gut microbiota and its derived metabolites improve immune homeostasis and prevent adverse cardiac remodelling and progression in heart failure?
Does modulation of the gut microbiota and its derived metabolites improve immune homeostasis and prevent adverse cardiac remodelling and progression in heart failure?
This narrative review synthesizes evidence on how gut microbiota and their metabolites (such as SCFAs, LPS, and TMAO) modulate innate and adaptive immune responses in post-infarction cardiac remodelling and heart failure, highlighting the gut microbiome as a promising therapeutic target.
Answers are grounded in this paper and cite their sources.
Microbiota-targeted immune modulation should not yet change HF practice; leaves open human trials of diet, probiotics and metabolites.
The immune system has long been recognized as a key driver in the progression of heart failure (HF). However, clinical trials targeting immune effectors have consistently failed to improve patient outcome across different HF aetiologies. The activation of the immune system in HF is complex, involving a broad network of pro-inflammatory and immune-modulating components, which complicates the identification of specific immune pathways suitable for therapeutic targeting. Increasing attention has been devoted to identifying gut microbial pathways that affect cardiac remodelling and metabolism and, thereby impacting the development of HF. In particular, gut microbiota-derived metabolites, absorbed by the host and transported to the peripheral circulation, can act as signalling molecules, influencing metabolism and immune homeostasis. Recent reports suggest that the gut microbiota plays a crucial role in modulating immune processes involved in HF. Here, we summarize recent advances in understanding the contributory role of gut microbiota in (auto-)immune pathways that critically determine the progression or alleviation of HF. We also thoroughly discuss potential gut microbiota-based intervention strategies to treat or decelerate HF progression.
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Roessler et al. (2024) studied this question.
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