Evidence map›Paper›PMID 26407987›Full record

ReviewImmunologic research2015

Chronic intermittent hypoxia exposure-induced atherosclerosis: a brief review.

Dongmei Song, Guoqiang Fang, Harly Greenberg, Shu Fang Liu

Abstract readComparative StudyReview
PubMed Publisher
In one paragraph

Review in Immunologic research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.5field-weighted citation impact, top 12% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

28 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Effect of aortic smooth muscle BK channels on mediating chronic intermittent hypoxia-induced vascular dysfunction.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2024
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  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
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  15. Article
  16. Article
  17. [Progress in obstructive sleep apnea and atherosclerosis].Lin chuang er bi yan hou tou jing wai ke za zhi = Journal of clinical otorhinolaryngology head and neck surgery · 2020
    Review
  18. Review
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 1 country.

Dongmei SongCenters for Heart and Lung Research, and Pulmonary, Critical Care and Sleep Medicine, The Feinstein Institute for Medical Research, Hofstra North Shore-LIJ School of Medicine, 350 Community Drive, Manhasset, NY, 11030, USA.
Guoqiang FangCenters for Heart and Lung Research, and Pulmonary, Critical Care and Sleep Medicine, The Feinstein Institute for Medical Research, Hofstra North Shore-LIJ School of Medicine, 350 Community Drive, Manhasset, NY, 11030, USA.
Harly GreenbergCenters for Heart and Lung Research, and Pulmonary, Critical Care and Sleep Medicine, The Feinstein Institute for Medical Research, Hofstra North Shore-LIJ School of Medicine, 350 Community Drive, Manhasset, NY, 11030, USA.
Shu Fang LiuCenters for Heart and Lung Research, and Pulmonary, Critical Care and Sleep Medicine, The Feinstein Institute for Medical Research, Hofstra North Shore-LIJ School of Medicine, 350 Community Drive, Manhasset, NY, 11030, USA. Sliu@nshs.edu.
Feinstein Institute for Medical Research · USHofstra University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Obstructive sleep apnea (OSA) is highly prevalent in the USA and is recognized as an independent risk factor for atherosclerotic cardiovascular disease. Identification of atherosclerosis risk factor attributable to OSA may provide opportunity to develop preventive measures for cardiovascular risk reduction. Chronic intermittent hypoxia (CIH) is a prominent feature of OSA pathophysiology and may be a major mechanism linking OSA to arteriosclerosis. Animal studies demonstrated that CIH exposure facilitated high-cholesterol diet (HCD)-induced atherosclerosis, accelerated the progression of existing atherosclerosis, and induced atherosclerotic lesions in the absence of other atherosclerosis risk factors, demonstrating that CIH is an independent causal factor of atherosclerosis. Comparative studies revealed major differences between CIH-induced and the classic HCD-induced atherosclerosis. Systemically, CIH was a much weaker inducer of atherosclerosis. CIH and HCD differentially activated inflammatory pathways. Histologically, CIH-induced atherosclerotic plaques had no clear necrotic core, contained a large number of CD31+ endothelial cells, and had mainly elastin deposition, whereas HCD-induced plaques had typical necrotic cores and fibrous caps, contained few endothelial cells, and had mainly collagen deposition. Metabolically, CIH caused mild, but HCD caused more severe dyslipidemia. Mechanistically, CIH did not, but HCD did, cause macrophage foam cell formation. NF-κB p50 gene deletion augmented CIH-induced, but not HCD-induced atherosclerosis. These differences reflect the intrinsic differences between the two types of atherosclerosis in terms of pathological nature and underlying mechanisms and support the notion that CIH-induced atherosclerosis is a new paradigm that differs from the classic HCD-induced atherosclerosis.

Indexed as

AnimalsAtherosclerosisCholesterol, DietaryCollagenDiet, AtherogenicDisease Models, AnimalElastinFoam CellsGene Knockout TechniquesHumansHypoxiaNF-kappa BRisk FactorsSignal TransductionSleep Apnea, ObstructiveCholesterol, DietaryCollagenElastinNF-kappa BAtherosclerosisChronic intermittent hypoxiaDyslipidemiaInflammationObstructive sleep apnea

Identifiers

PMID26407987
OpenAlexW1786914917

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.