Evidence map›Paper›PMID 36422496›Full record

ArticleTurkish journal of medical sciences2022

Impact of ATP synthase/coupling factor 6 in hypoxic pulmonary arterial hypertension: An experimental rat model.

Nannan Lı, Yugen Shı, Jie Yın, Li Sun, Qingshan Zhang, Shuai Bao, Juan Zhang, Youlei Lı, Miaomiao Wang, Yanwei Zhang and 5 more

Open access · bronzeAbstract read
In one paragraph

Article in Turkish journal of medical sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.2field-weighted citation impact, top 51% 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

2 citing papers in PubMed, 2 citations in OpenAlex.

  1. Article
  2. Review
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

15 authors at 1 institution in 1 country.

Nannan LıDepartment of Chinese Medicine Ophthalmology, the First Affiliated Hospital of Shandong First Medical University, Shandong, China.
Yugen ShıDepartment of Cardiology, The First Affiliated Hospital of Shandong First Medical University - Shandong Provincial Qianfoshan Hospital, Shandong Medicine and Health Key Laboratory of Cardiac Electrophysiology and Arrhythmia, Shandong, China.
Jie YınDepartment of Cardiology, The First Affiliated Hospital of Shandong First Medical University - Shandong Provincial Qianfoshan Hospital, Shandong Medicine and Health Key Laboratory of Cardiac Electrophysiology and Arrhythmia, Shandong, China.
Li SunDepartment of Emergency Medicine, The First Affiliated Hospital of Shandong First Medical University - Shandong Provincial Qianfoshan Hospital, Shandong Medicine and Health Key Laboratory of Emergency Medicine, Shandong, China.
Qingshan ZhangDepartment of Emergency Medicine, The First Affiliated Hospital of Shandong First Medical University - Shandong Provincial Qianfoshan Hospital, Shandong Medicine and Health Key Laboratory of Emergency Medicine, Shandong, China.
Shuai BaoDepartment of Emergency Medicine, Shandong Provincial Qianfoshan Hospital, Shandong University, Shandong, China.
Juan ZhangDepartment of Intensive Care Unit, The First Affiliated Hospital of University of Science and Technology of China, Anhui, China.
Youlei LıDepartment of Emergency, People's Hospital of Xia Jin, Dezhou, China.
Miaomiao WangDepartment of Emergency, Shandong First Medical University, Shandong, China.
Yanwei ZhangDepartment of Emergency, Shandong First Medical University, Shandong, China.
Mei XueDepartment of Emergency Medicine, The First Affiliated Hospital of Shandong First Medical University - Shandong Provincial Qianfoshan Hospital, Shandong Medicine and Health Key Laboratory of Emergency Medicine, Shandong, China.
Lei QıDepartment of Cardiology, The First Affiliated Hospital of Shandong First Medical University - Shandong Provincial Qianfoshan.
Yan Lıedical Research Center, Shandong Provincial Qianfoshan Hospital, the First Hospital Affiliated with Shandong First Medical University, Shandong, China.
Suhua YanDepartment of Cardiology, The First Affiliated Hospital of Shandong First Medical University - Shandong Provincial Qianfoshan Hospital, Shandong Medicine and Health Key Laboratory of Cardiac Electrophysiology and Arrhythmia, Shandong, China.
Xiaolu LıDepartment of Emergency Medicine, The First Affiliated Hospital of Shandong First Medical University - Shandong Provincial Qianfoshan Hospital, Shandong Medicine and Health Key Laboratory of Emergency Medicine, Shandong, China.
Shandong First Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHypoxia-induced pulmonary arterial hypertension (PAH) is characterized by prostacyclin (PGI2 ) disorder, which manifests in the same manner as in monocrotaline (MCT)-induced PAH. Endogenous PGI2 inhibitor coupling factor 6 (CF6) is involved in MCT-induced PAH. This study aimed to explore the presence or absence of a correlation between hypoxia-induced PAH and CF6.

methodsThis study was conducted between January 2019 and June 2020. A total of 135 male Wistar rats (aged 8 weeks and weighing 200-250 g) were randomly divided into five groups: (A) control, (B) 1 week of hypoxia, (C) 2 weeks of hypoxia, (D) 3 weeks of hypoxia, and (E) 4 weeks of hypoxia. CF6 expression in both lung tissue and blood samples from the lung vasculature and tail vein was measured by western blotting, immunohistochemistry, reverse transcription polymerase chain reaction, and enzyme-linked immunosorbent assay.

resultsHemodynamic and morphological changes in hypoxia-induced rats indicated PAH development. The results showed the presence of a correlation between the mRNA and protein levels of CF6 in lung tissue, activity of mitochondrial ATP synthase, and hypoxia time, and there was a significant increment in the group exposed to hypoxia for 4 weeks compared to the control group. The decrement expression of ATPase inhibitory factor 1 (IF 1) mRNA was consistent with the outcomes of ATP synthase activity in lung tissue in the 4 weeks of hypoxia group compared with the control group. However, the levels of CF6 and ATP synthase activity did not differ between blood samples from the lung vasculature and tail vein. DISCUSSION: : In hypoxia-induced PAH, CF6 showed downregulated expression in lung tissue, but not in pulmonary vasculature and circulation. Therefore, we speculated that CF6 and ATP synthase may play important roles in hypoxia-induced PAH.

Indexed as

Hypertension, PulmonaryPulmonary Arterial HypertensionAdenosine TriphosphateAnimalsHypoxiaMaleMitochondrial Proton-Translocating ATPasesMonocrotalineOxidative Phosphorylation Coupling FactorsRatsRats, WistarRNA, MessengerAdenosine TriphosphateF(6) ATPaseMitochondrial Proton-Translocating ATPasesMonocrotalineOxidative Phosphorylation Coupling FactorsRNA, Messengeradenosine triphosphate synthase activityCoupling factor 6hypoxicpulmonary arterial hypertension

Identifiers

PMID36422496
PMCPMC10395693
OpenAlexW4310329963

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.