ArticleBasic research in cardiology2026
Spinal neuronal TLR4-induced enhancement of nociceptive signals contributes to myocardial ischemia/reperfusion injury.
Article in Basic research in cardiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors.
Funding
Abstract
Myocardial ischemia/reperfusion (I/R) injury has been extensively studied, yet the underlying neuroinflammatory mechanisms are not fully understood. While toll-like receptor 4 (TLR4) is known to be involved in neuropathic pain and neurodegeneration, its role in the central nervous system during myocardial I/R injury, as well as how it modulates neuronal activity to influence cardiac function, remains unclear. In this study, we established a rodent model of myocardial I/R injury by ligating the left anterior descending artery. We found that myocardial I/R injury significantly upregulated TLR4 expression in the spinal dorsal horn, with enhanced TLR4 levels predominantly localized to spinal neurons rather than astrocytes or microglia. Upregulation of TLR4 exhibited functional crosstalk with the calcitonin gene-related peptide (CGRP) receptor, facilitating the transmission of nociceptive signals from the injured myocardium and leading to hyperexcitation of spinal neurons. Both pharmacological inhibition and genetic manipulation of TLR4 signaling resulted in a marked reduction in neuronal activity and attenuated myocardial ischemic injury, accompanied by decreased nociceptive input from the heart to the spinal dorsal horn. Collectively, our findings reveal classic neuroinflammatory signals derived from TLR4 that contribute to neuronal hyperexcitation following myocardial I/R injury. Targeting spinal neuronal TLR4 signaling represents a promising therapeutic strategy for patients with acute myocardial injury.
Indexed as
Identifiers
42821069What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.