Evidence map›Paper›PMID 27924067›Full record

ArticleJournal of biomedical research2016

Chronic intermittent hypoxia induces cardiac inflammation and dysfunction in a rat obstructive sleep apnea model.

Qin Wei, Yeping Bian, Fuchao Yu, Qiang Zhang, Guanghao Zhang, Yang Li, Songsong Song, Xiaomei Ren, Jiayi Tong

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of biomedical research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

34 citing papers in PubMed, 59 citations in OpenAlex.

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  17. Elevated serum matrix metalloproteinase-2 levels in heart failure patients with reduced ejection fraction and Cheyne-Stokes respiration.Journal of clinical sleep medicine : JCSM : official publication of the American Academy of Sleep Medicine · 2022
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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

9 authors at 3 institutions in 1 country.

Qin WeiCardiovascular Institute, Southeast University, Nanjing, Jiangsu 210009, China.
Yeping BianDepartment of Intensive Care Unit, Jiangsu Province Official Hospital, Nanjing, Jiangsu 210009, China.
Fuchao YuCardiovascular Institute, Southeast University, Nanjing, Jiangsu 210009, China.
Qiang ZhangDepartment of Cardiology, Zhongda Hospital Affiliated to Southeast University, Nanjing, Jiangsu 210009, China.
Guanghao ZhangCardiovascular Institute, Southeast University, Nanjing, Jiangsu 210009, China.
Yang LiCardiovascular Institute, Southeast University, Nanjing, Jiangsu 210009, China.
Songsong SongCardiovascular Institute, Southeast University, Nanjing, Jiangsu 210009, China.
Xiaomei RenDepartment of Geriatrics, Zhongda Hospital Affiliated to Southeast University, Nanjing, Jiangsu 210009, China.
Jiayi TongCardiovascular Institute, Southeast University, Nanjing, Jiangsu 210009, China.
Zhongda Hospital Southeast University · CNSoutheast University · CNJiangsu Province Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic intermittent hypoxia is considered to play an important role in cardiovascular pathogenesis during the development of obstructive sleep apnea (OSA). We used a well-described OSA rat model induced with simultaneous intermittent hypoxia. Male Sprague Dawley rats were individually placed into plexiglass chambers with air pressure and components were electronically controlled. The rats were exposed to intermittent hypoxia 8 hours daily for 5 weeks. The changes of cardiac structure and function were examined by ultrasound. The cardiac pathology, apoptosis, and fibrosis were analyzed by H&E staining, TUNNEL assay, and picosirius staining, respectively. The expression of inflammation and fibrosis marker genes was analyzed by quantitative real-time PCR and Western blot. Chronic intermittent hypoxia/low pressure resulted in significant increase of left ventricular internal diameters (LVIDs), end-systolic volume (ESV), end-diastolic volume (EDV), and blood lactate level and marked reduction in ejection fraction and fractional shortening. Chronic intermittent hypoxia increased TUNNEL-positive myocytes, disrupted normal arrangement of cardiac fibers, and increased Sirius stained collagen fibers. The expression levels of hypoxia induced factor (HIF)-1α, NF-kB, IL-6, and matrix metallopeptidase 2 (MMP-2) were significantly increased in the heart of rats exposed to chronic intermittent hypoxia. In conclusion, the left ventricular function was adversely affected by chronic intermittent hypoxia, which is associated with increased expression of HIF-1α and NF-kB signaling molecules and development of cardiac inflammation, apoptosis and fibrosis.

Indexed as

cardiac dysfunctioninflammationmodel chronic intermittent hypoxiaobstructive sleep apnea

Identifiers

PMID27924067
PMCPMC5138581
OpenAlexW2578655772

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.