2026-01-27 カリフォルニア大学サンディエゴ校(UCSD)
<関連情報>
- https://today.ucsd.edu/story/new-research-connects-heart-attacks-to-brain-nervous-and-immune-systems
- https://www.cell.com/cell/fulltext/S0092-8674(25)01506-5
心筋梗塞の根底にある三重節心臓脳神経免疫ループ A triple-node heart-brain neuroimmune loop underlying myocardial infarction
Saurabh Yadav ∙ Van K. Ninh ∙ Jonathan W. Lovelace ∙ … ∙ Ruchi Sehgal ∙ Kevin R. King ∙ Vineet Augustine
Cell Published:January 27, 2026
DOI:https://doi.org/10.1016/j.cell.2025.12.058
Graphical abstract

Highlights
- TRPV1 vagal sensory neuronal ablation (node 1) improves cardiac function post MI
- TRPV1 vagal sensory neuronal ablation fortifies the border zone against injury after MI
- PVN AT1aR neuronal inhibition (node 2) improves cardiac function post MI
- Superior cervical ganglia IL-1β immune block (node 3) improves cardiac function post MI
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.

