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Heart–brain axis

Neuroimmune circuits drive pathological remodelling after myocardial infarction

Nature Reviews Cardiology (2026)Cite this article

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A heart–brain loop, which involves vagal sensory neurons (VSNs) in the heart, the paraventricular nucleus (PVN) in the brain and sympathetic signalling via the superior cervical ganglia (SCG), mediates adverse cardiac remodelling after myocardial infarction (MI) in mice. Of note, inhibition of pro-inflammatory IL-1β signalling in the SCG substantially reduced the cardiac complications after MI in these mice. These findings come from a new study published by Vineet Augustine and colleagues in Cell. “Our findings reframe MIs as a disorder of nervous–immune system communication rather than simply a failure of cardiac tissue,” comments Augustine.

VSNs transmit information from the heart to the brain. The researchers identified a unique subset of TRPV1+ VSNs in the ventricles whose expression was increased after MI in mice. Targeted ablation of these neurons after MI reduced infarct size, improved ejection fraction, diminished sympathetic innervation and decreased inflammation.

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  • Valenza, G. et al. The brain–heart axis: integrative cooperation of neural, mechanical and biochemical pathways. Nat. Rev. Cardiol. 22, 537–550 (2025)

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  1. Nature Reviews Cardiology http://www.nature.com/nrcardio/

    Gregory B. Lim

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  1. Gregory B. Lim
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Correspondence to Gregory B. Lim.

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Lim, G.B. Neuroimmune circuits drive pathological remodelling after myocardial infarction. Nat Rev Cardiol (2026). https://doi.org/10.1038/s41569-026-01258-y

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