ArticleCardiology journal2019
High mobility group box-1 in hypothalamic paraventricular nuclei attenuates sympathetic tone in rats at post-myocardial infarction.
Article in Cardiology journal, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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
4 citing papers in PubMed, 5 citations in OpenAlex.
- P300-Targeted Acetylome Reveals a Role for HMGB1 Translocation in Central Cardiac Sympathetic Activation Post Myocardial Infarction.Journal of inflammation research · 2025Article
- Asprosin in the Paraventricular Nucleus Induces Sympathetic Activation and Pressor Responses via cAMP-Dependent ROS Production.International journal of molecular sciences · 2022Article
- Monosynaptic Input Mapping of Diencephalic Projections to the Cerebrospinal Fluid-Contacting Nucleus in the Rat.Frontiers in neuroanatomy · 2020Article
- TLR4 participates in sympathetic hyperactivity Post-MI in the PVN by regulating NF-κB pathway and ROS production.Redox biology · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundInflammation is associated with increased sympathetic drive in cardiovascular diseases. The paraventricular nucleus (PVN) of the hypothalamus is a key regulator of sympathetic nerve activity at post-myocardial infarction (MI). High mobility group box-1 (HMGB1) exhibits inflammatory cytokine like activity in the extracellular space. Inflammation is associated with increased sympathetic drive in cardiovscular diseases. However, the role of HMGB1 in sympathetic nerve activity at post-MI remains unknown. The aim of the present study is to determine the role and mechanism of HMGB1 in the PVN, in terms of sympathetic activity and arrhythmia after MI.
methodsSprague-Dawley rats underwent left anterior descending coronary artery ligation to induce MI. Anti-HMGB1 polyclonal antibody or control IgG was bilaterally microinjected into the PVN (5 μL every second day for seven consecutive days). Then, renal sympathetic nerve activity (RSNA) was recorded. The association between ventricular arrhythmias (VAs) and MI was evaluated using programmed electrophysiological stimulation. After performing electrophysiological experiments in vivo, immunohistochemistry was used to detect the distribution of HMGB1, while Western blot was used to detect the expression of HMGB1 and p-ERK in the PVN of MI rats.
resultsHMGB1 and p-ERK were upregulated in the PVN in rats at post-MI. Moreover, bilateral PVN microinjection of anti-HMGB1 polyclonal antibody reversed the expression of HMGB1 and p-ERK, and consequently decreased the baseline RSNA and inducible VAs, when compared to those in sham rats.
conclusionsThese results suggest that MI causes the translocation of HMGB1 in the PVN, which leads to sympathetic overactivation through the ERK1/2 signaling pathway. The bilateral PVN microinjection of anti-HMGB1 antibody can be an effective therapy for MI-induced arrhythmia.
Indexed as
Identifiers
What 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.