ArticleAnnals of medicine2025
Sleep fragmentation exacerbates myocardial ischemia-reperfusion injury via hypothalamic paraventricular nucleus-resident OX1R-mediated sympathetic hyperactivity in adult mice.
Article in Annals of medicine, 2025. 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
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND/
objectiveSleep fragmentation (SF) is a prevalent sleep disorder with an increased risk of cardiovascular diseases. Although epidemiological studies have shown a strong link between SF and adverse cardiac outcomes, specific central neural mechanisms through which SF exacerbates myocardial ischemia-reperfusion injury (MI/RI) are unclear. This study investigated the role of orexin receptor 1 (OX1R) in the hypothalamic paraventricular nucleus (PVN) in SF-induced aggravation of MI/RI and the underlying mechanism using a mouse model. MATERIALS AND
methodsC57BL/6 mice were subjected to chronic SF for 16 weeks before MI/RI modeling. Cardiac function was assessed by echocardiography. Sympathetic activity was evaluated based on the heart rate variability analysis. Molecular changes were evaluated by western blotting, qRT-PCR, and immunohistochemistry. The
resultsSF mice exhibited significantly worse cardiac dysfunction and larger infarct areas following MI/RI compared to the controls. This was accompanied by enhanced sympathetic nerve activity and elevated catecholamine levels. Specifically, SF upregulated OX1R expression in the PVN and increased the levels of neuronal activation markers such as c-Fos. Pharmacological blockade of OX1R in the PVN significantly ameliorated SF-induced cardiac dysfunction, reduced the infarct size, and suppressed sympathetic hyperactivity post-MI/RI.
conclusionsSF may aggravate MI/RI through PVN OX1R-associated sympathetic hyperactivation. Pharmacological inhibition of OX1R improved cardiac outcomes, supporting the involvement of the PVN OX1R-sympathetic pathway in sleep disruption related cardiac injury.
Indexed as
Identifiers
What Socratic 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 Socratic graph.