ReviewPatient preference and adherence2013
Obstructive sleep apnea and endothelial progenitor cells.
Review in Patient preference and adherence, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.
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
11 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.
- Leptin and leptin receptor gene polymorphisms in obstructive sleep apnea: a HuGE review and meta-analysis.Sleep & breathing = Schlaf & Atmung · 2015Pooled it
- Endothelial Dysfunction and Cardiovascular Risk in Obstructive Sleep Apnea: A Review Article.Life (Basel, Switzerland) · 2022Review
- Obstructive Sleep Apnea as a Risk Factor for Venous Thromboembolism: A Systematic Review.Cureus · 2022Review
- Oxidative Stress and Inflammation Biomarker Expression in Obstructive Sleep Apnea Patients.Journal of clinical medicine · 2021Review
- The Association of Nephroblastoma Overexpressed (NOV) and Endothelial Progenitor Cells with Oxidative Stress in Obstructive Sleep Apnea.Oxidative medicine and cellular longevity · 2021Article
- Reassessing the effects of continuous positive airway pressure (CPAP) on arterial stiffness and peripheral blood derived CD34+ progenitor cells in subjects with sleep apnea.Stem cell research & therapy · 2019Article
- Reduced gray matter volume and respiratory dysfunction in Parkinson's disease: a voxel-based morphometry study.BMC neurology · 2018Article
- Sustained apnea induces endothelial activation.Clinical cardiology · 2017Article
- Obstructive sleep apnea and hormones - a novel insight.Archives of medical science : AMS · 2017Article
- Re-evaluation of the WHO (2010) formaldehyde indoor air quality guideline for cancer risk assessment.Archives of toxicology · 2017Review
- Stem/progenitor cells and obstructive sleep apnea syndrome - new insights for clinical applications.World journal of stem cells · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundObstructive sleep apnea (OSA) occurs in 4% of middle-aged men and 2% of middle-aged women in the general population, and the prevalence is even higher in specific patient groups. OSA is an independent risk factor for a variety of cardiovascular diseases. Endothelial injury could be the pivotal determinant in the development of cardiovascular pathology in OSA. Endothelial damage ultimately represents a dynamic balance between the magnitude of injury and the capacity for repair. Bone marrow-derived endothelial progenitor cells (EPCs) within adult peripheral blood present a possible means of vascular maintenance that could home to sites of injury and restore endothelial integrity and normal function.
methodsWe summarized pathogenetic mechanisms of OSA and searched for available studies on numbers and functions of EPCs in patients with OSA to explore the potential links between the numbers and functions of EPCs and OSA. In particular, we tried to elucidate the molecular mechanisms of the effects of OSA on EPCs.
conclusionIntermittent hypoxia cycles and sleep fragmentation are major pathophysiologic characters of OSA. Intermittent hypoxia acts as a trigger of oxidative stress, systemic inflammation, and sympathetic activation. Sleep fragmentation is associated with a burst of sympathetic activation and systemic inflammation. In most studies, a reduction in circulating EPCs has emerged. The possible mechanisms underlying the decrease in the number or function of EPCs include prolonged inflammation response, oxidative stress, increased sympathetic activation, physiological adaptive responses of tissue to hypoxia, reduced EPC mobilization, EPC apoptosis, and functional impairment in untreated OSA. Continuous positive airway pressure (CPAP) therapy for OSA affects the mobilization, apoptosis, and function of EPCs through preventing intermittent hypoxia episodes, improving sleep quality, and reducing systemic inflammation, oxidative stress levels, and sympathetic overactivation. To improve CPAP adherence, the medical staff should pay attention to making the titration trial a comfortable first CPAP experience for the patients; for example, using the most appropriate ventilators or proper humidification. It is also important to give the patients education and support about CPAP use in the follow-up, especially in the early stage of the treatment.
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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.