A triple-node heart-brain neuroimmune loop underlying myocardial infarction

[poetinsf]

Another paper about the brain and the immune system effecting each other. In gist, ablating the neurons activated by the heat attack improved the recovery of heart muscle in mice. Might have relevance to MECFS neuroimmune hypothesis.

Summary​

Myocardial infarction (MI) triggers adverse cardiac events, immune responses, and nervous system activation, but the neural and neuroimmune mechanisms remain understudied. Using single-cell RNA sequencing (scRNA-seq) and tissue clearing, we identified transient receptor potential vanilloid-1 (TRPV1)-expressing vagal sensory neurons (VSNs) that increase ventricular innervation post MI. Ablating these VSNs mitigated MI pathology, reducing infarct size, abnormal electrocardiograms, cardiac dysfunction, sympathetic innervation, and pro-inflammatory cytokine interleukin 1β (IL-1β). Single-nuclei RNA-seq (snRNA-seq) and spatial transcriptomics revealed reduced border zone expansion in MI hearts following VSN ablation. Tracing the effects to the brain, we found that MI activated angiotensin II receptor type 1 (AT1aR)-expressing neurons in the paraventricular nucleus (PVN), whose inhibition mirrored benefits of TRPV1 VSN ablation. Additionally, the superior cervical ganglia (SCGs) exhibited intensified post-MI sympathetic innervation and IL-1β signaling. Blocking IL-1β in the SCG significantly reduced complications post MI. This study reveals a triple-node heart-brain loop underlying MI and potential therapeutic targets

Paper: https://www.cell.com/cell/fulltext/S0092-8674(25)01506-5?rss=yes

Article: https://www.npr.org/2026/01/27/nx-s1-5690108/heart-attack-brain-nervous-immune-system