ArticleOncotarget2017
Chronic inflammation and apoptosis propagate in ischemic cerebellum and heart of non-human primates.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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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
11 citing papers in PubMed, 23 citations in OpenAlex.
- Post-stroke Arrhythmias: Performance of Brain-heart Crosstalk Networks.Current cardiology reviews · 2025Review
- Stroke-heart syndrome: current progress and future outlook.Journal of neurology · 2024Review
- Stroke Related Brain-Heart Crosstalk: Pathophysiology, Clinical Implications, and Underlying Mechanisms.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Review
- Article
- Peripheral Organ Injury After Stroke.Frontiers in immunology · 2022Review
- Withania coagulans extract attenuates oxidative stress-mediated apoptosis of cerebellar purkinje neurons after ischemia/reperfusion injury.Metabolic brain disease · 2021Article
- Cerebral-Cardiac Syndrome and Diabetes: Cardiac Damage After Ischemic Stroke in Diabetic State.Frontiers in immunology · 2021Review
- Macrophage-NLRP3 Inflammasome Activation Exacerbates Cardiac Dysfunction after Ischemic Stroke in a Mouse Model of Diabetes.Neuroscience bulletin · 2020Article
- Spleen participation in partial MHC class II construct neuroprotection in stroke.CNS neuroscience & therapeutics · 2020Review
- Relative Resilience of Cerebellar Purkinje Cells in a Cardiac Arrest/Resuscitation Rat Model.Neurocritical care · 2020Article
- Brain-heart interaction after acute ischemic stroke.Critical care (London, England) · 2020Review
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 1 institution in 1 country.
Funding
Abstract
The major pathological consequences of cerebral ischemia are characterized by neurological deficits commonly ascribed to the infarcted tissue and its surrounding region, however, brain areas, as well as peripheral organs, distal from the original injury may manifest as subtle disease sequelae that can increase the risks of co-morbidities complicating the disease symptoms. To evaluate the vulnerability of the cerebellum and the heart to secondary injuries in the late stage of transient global ischemia (TGI) model in non-human primates (NHP), brain and heart tissues were collected at six months post-TGI. Unbiased stereological analyses of immunostained tissues showed significant Purkinje cells loss in lobule III and lobule IX of the TGI cerebellum relative to sham cerebellum, with corresponding upregulation of inflammatory and apoptotic cells. Similarly, TGI hearts revealed significant activation of inflammatory and apoptotic cells relative to sham hearts. Aberrant inflammation and apoptosis in the cerebellum and the heart of chronic TGI-exposed NHPs suggest distal secondary injuries manifesting both centrally and peripherally. These results advance our understanding on the sustained propagation of chronic secondary injuries after TGI, highlighting the need to develop therapeutic interventions targeting the brain, as well as the heart, in order to abrogate cerebral ischemia and its related co-morbidities.
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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.