Evidence map›Paper›PMID 28560002›Full record

ArticleAmerican journal of translational research2017

Prostaglandin E1 protects coronary microvascular function via the glycogen synthase kinase 3β-mitochondrial permeability transition pore pathway in rat hearts subjected to sodium laurate-induced coronary microembolization.

Houyong Zhu, Yu Ding, Xiaoqun Xu, Meiya Li, Yangliang Fang, Beibei Gao, Hengyi Mao, Guoxin Tong, Liang Zhou, Jinyu Huang

Open access · greenAbstract read
In one paragraph

Article in American journal of translational research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.6field-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

19 citing papers in PubMed, 20 citations in OpenAlex.

  1. Prostaglandin EFrontiers in medicine · 2026
    Review
  2. Article
  3. Article
  4. Article
  5. A fresh look at coronary microembolization.Nature reviews. Cardiology · 2022
    Review
  6. Pretreatment with Shenmai Injection Protects against Coronary Microvascular Dysfunction.Evidence-based complementary and alternative medicine : eCAM · 2022
    Article
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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

10 authors at 3 institutions in 1 country.

Houyong ZhuZhejiang Chinese Medical UniversityChina.
Yu DingDepartment of Cardiology, Hangzhou First People's Hospital, Nanjing Medical UniversityHangzhou, China.
Xiaoqun XuZhejiang Chinese Medical UniversityChina.
Meiya LiZhejiang Chinese Medical UniversityChina.
Yangliang FangZhejiang Chinese Medical UniversityChina.
Beibei GaoDepartment of Cardiology, Hangzhou First People's Hospital, Nanjing Medical UniversityHangzhou, China.
Hengyi MaoNanjing Medical UniversityChina.
Guoxin TongDepartment of Cardiology, Hangzhou First People's Hospital, Nanjing Medical UniversityHangzhou, China.
Liang ZhouDepartment of Cardiology, Hangzhou First People's Hospital, Nanjing Medical UniversityHangzhou, China.
Jinyu HuangDepartment of Cardiology, Hangzhou First People's Hospital, Nanjing Medical UniversityHangzhou, China.
Hangzhou First People's Hospital · CNZhejiang Chinese Medical University · CNNanjing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Prostaglandin E1 (PGE1) is used as a pretreatment for ischemia reperfusion injury in many biological systems. However, its value as a pretreatment for coronary microembolization (CME) is unknown. The goal of this study was to determine whether PGE1 would protect against CME. In a CME rat model, we observed microthrombi and early myocardial ischemia, with endothelium appearing exfoliated and mitochondria having irregular morphology and decreased internal complexity. The level of fibrinogen-like protein 2 prothrombinase was increased and superoxide dismutase and catalase levels were decreased. Moreover, mitochondria copy number and mitochondrial permeability transition pore (mPTP) opening were increased. Pretreatment with PGE1 (1 or 2 μg/kg) significantly improved these cardiological deficits, acting via the glycogen synthase kinase 3β (GSK-3β)-mPTP pathway. Unexpectedly, the phosphorylation of Akt at Ser473 decreased in the PGE1 at high dose. Overall, our findings suggested an important role for PGE1 in pretreatment of coronary microvascular dysfunction.

Indexed as

AktCoronary microembolizationcoronary microvascular dysfunctionGSK-3βmitochondrial permeability transition poreprostaglandin E1sodium laurate

Identifiers

PMID28560002
PMCPMC5446534
OpenAlexW2997274745

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.