What is the clinical evidence from this study?

Study design: Other. Population: Myocardial ischemia-reperfusion injury. Intervention: Chronic pain vs. No chronic pain. Primary outcome: Myocardial infarction area, endothelial cell apoptosis and inflammation.

What does this research mean for the field?

Chronic pain exacerbates myocardial ischemia-reperfusion injury by increasing sympathetic nerve tone, which drives endothelial cell apoptosis and inflammation via the NLRP3 pathway. Novelty: ClaimNovelty.NOVEL_FINDING. Consensus alignment: ConsensusAlignment.NEUTRAL.

What question did this study set out to answer?

To investigate the mechanisms by which chronic pain and increased sympathetic tone exacerbate myocardial ischemia-reperfusion injury.

September 14, 2026Clinical ScienceOpen Access

Elevated sympathetic tone exacerbates myocardial ischemia reperfusion injury through enhancing endothelial cell inflammation and apoptosis in chronic pain mice

View Full Paper

Ask AI

Bookmark

Key result

Chronic pain exacerbates myocardial ischemia-reperfusion injury via the sympathetic-NLRP3 pathway.

Why the study?

Extensive evidence links chronic pain to an increased cardiovascular risk, but its direct impact on myocardial ischemia-reperfusion remains poorly understood.

Population

Young male mice with chronic constriction injury-induced chronic pain subjected to MI/R

Comparison

Chemical sympathectomy with 6-OHDA, SCG ablation, MCC950, or bisoprolol vs controls

Design

Preclinical animal study

Authors

MTMi TianFoshan University CZChengrui ZhuangFoshan University JHJian HeFoshan University

Discussion

Member takes

Implication

May link chronic pain to worse ischemia-reperfusion injury via sympathetic-NLRP3 in mice; leaves open human translation and therapeutic targeting.

Key Points

To investigate the mechanisms by which chronic pain and increased sympathetic tone exacerbate myocardial ischemia-reperfusion injury.
Induced chronic pain in young male mice via chronic constriction injury (CCI) of the brachial plexus prior to myocardial ischemia-reperfusion.
Mapped and assessed the superior cervical ganglion (SCG)-cardiac neural circuit using viral tracing, c-Fos staining, and heart rate variability monitoring.
Administered 6-hydroxydopamine for chemical sympathectomy, MCC950 for NLRP3 inflammasome inhibition, and bisoprolol for beta-blockade.
Chronic pain significantly expanded myocardial infarction size and increased sympathetic nerve tone, endothelial cell inflammation, and apoptosis.
SCG-cardiac circuit hyperactivation drove injury, whereas chemical ablation of the SCG using 6-hydroxydopamine attenuated endothelial apoptosis and myocardial damage.
Pharmacological inhibition of the NLRP3 inflammasome via MCC950 or sympathetic suppression using bisoprolol reduced endothelial apoptosis, inflammation, and myocardial infarction area.

Structured PICO

Population

Young male mice subjected to chronic constriction injury of the brachial plexus to induce chronic pain prior to myocardial ischemia-reperfusion.

Exposure

Chemical sympathectomy using 6-hydroxydopamine (6-OHDA), ablation of superior cervical ganglion (SCG), MCC950 (NLRP3 inhibitor), or bisoprolol

Comparator

Control mice (implied vehicle or sham)

Outcome

Myocardial infarction area, endothelial cell apoptosis, and inflammationsurrogate

Chronic pain exacerbates myocardial ischemia-reperfusion injury through a sympathetic-NLRP3 inflammatory pathway, highlighting a mechanistic link between chronic pain and cardiovascular risk.

Limitations

Data were obtained exclusively from young male mice, warranting validation in female, aged, and clinically relevant models.
Data obtained exclusively from young male mice
Findings warrant validation in female, aged, and clinically relevant models

Cite This Study

Tian et al. (2026) studied Myocardial ischemia-reperfusion injury. Chronic pain vs. No chronic pain was evaluated on Myocardial infarction area, endothelial cell apoptosis and inflammation. Chronic pain exacerbated myocardial ischemia-reperfusion injury by increasing myocardial infarction area, endothelial cell apoptosis, and inflammation via the sympathetic-NLRP3 pathway.

synapsesocial.com/papers/6aa7b2890926e14a848b0fa2 https://doi.org/10.1042/cs20260983

View Full Paper

Ask AI

Bookmark

Implication

May link chronic pain to worse ischemia-reperfusion injury via sympathetic-NLRP3 in mice; leaves open human translation and therapeutic targeting.

Elevated sympathetic tone exacerbates myocardial ischemia reperfusion injury through enhancing endothelial cell inflammation and apoptosis in chronic pain mice

Discussion

Member takes

Implication

Key Points

Structured PICO

Limitations

Cite This Study

Elevated sympathetic tone exacerbates myocardial ischemia reperfusion injury through enhancing endothelial cell inflammation and apoptosis in chronic pain mice

Discussion

Member takes

Implication

Key Points

Structured PICO

Limitations

Cite This Study

Also Consider

Also Consider