Evidence map›Paper›PMID 32140105›Full record

ArticleFrontiers in pharmacology2020

Deferoxamine Treatment Combined With Sevoflurane Postconditioning Attenuates Myocardial Ischemia-Reperfusion Injury by Restoring HIF-1/BNIP3-Mediated Mitochondrial Autophagy in GK Rats.

Long Yang, Peng Xie, Jianjiang Wu, Jin Yu, Xin Li, Haiping Ma, Tian Yu, Haiying Wang, Jianrong Ye, Jiang Wang and 1 more

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

Article in Frontiers in pharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
4.6field-weighted citation impact, top 4% 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

31 citing papers in PubMed, 52 citations in OpenAlex.

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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

11 authors at 2 institutions in 1 country.

Long YangDepartment of Anesthesiology, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, China.
Peng XieGuizhou Key Laboratory of Anesthesia and Organ Protection, Department of Anesthesiology, Zunyi Medical College, Zunyi, China.
Jianjiang WuDepartment of Anesthesiology, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, China.
Jin YuDepartment of Anesthesiology, Chongqing Health Center for Women and Children, Chongqing, China.
Xin LiDepartment of Anesthesiology, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, China.
Haiping MaDepartment of Anesthesiology, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, China.
Tian YuGuizhou Key Laboratory of Anesthesia and Organ Protection, Department of Anesthesiology, Zunyi Medical College, Zunyi, China.
Haiying WangGuizhou Key Laboratory of Anesthesia and Organ Protection, Department of Anesthesiology, Zunyi Medical College, Zunyi, China.
Jianrong YeDepartment of Anesthesiology, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, China.
Jiang WangDepartment of Anesthesiology, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, China.
Hong ZhengDepartment of Anesthesiology, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, China.
First Affiliated Hospital of Xinjiang Medical University · CNZunyi Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondrial autophagy is involved in myocardial protection of sevoflurane postconditioning (SPostC) and in diabetic state this protective effect is weakened due to impaired HIF-1 signaling pathway. Previous studies have proved that deferoxamine (DFO) could activate impaired HIF-1α in diabetic state to restore the cardioprotective of sevoflurane, while the specific mechanism is unclear. This study aims to investigate whether HIF-1/BNIP3-mediated mitochondrial autophagy is involved in the restoration of sevoflurane postconditioning cardioprotection in diabetic state. Ischemia/reperfusion (I/R) model was established by ligating the anterior descending coronary artery and sevoflurane was administered at the first 15 min of reperfusion. Myocardial infarct size, mitochondrial ultrastructure and autophagosome, ATP content, mitochondrial membrane potential, ROS production, HIF-1α, BNIP3, LC3B-II, Beclin-1, P62, LAMP2 protein expression were detected 2 h after reperfusion, and cardiac function was evaluated by ultrasound at 24 h after reperfusion. Our results showed that with DFO treatment, SPostC up-regulated the expression of HIF-1α and BNIP3, thus reduced the expression of key autophagy proteins LC3B-II, Beclin-1, p62, and increased the expression of LAMP2. Furthermore, it reduced the accumulation of autophagosomes and ROS production, increased the content of ATP, and stabilized the membrane potential. Finally, the myocardial infarction size was reduced and cardiac function was improved. Taken together, DFO treatment combined with SPostC could alleviate myocardial ischemia reperfusion injury in diabetic rats by restoring and promoting HIF-1/BNIP3-mediated mitochondrial autophagy.

Indexed as

diabeteshypoxia-inducible factor-1ischemia-reperfusionmitochondrial autophagysevoflurane postconditioning

Identifiers

PMID32140105
PMCPMC7042377
OpenAlexW3006825624

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Registered trials

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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.