Evidence map›Paper›PMID 29962953›Full record

ArticleFrontiers in pharmacology2018

Sirt1 Activation by Post-ischemic Treatment With Lumbrokinase Protects Against Myocardial Ischemia-Reperfusion Injury.

Yi-Hsin Wang, Shun-An Li, Chao-Hsin Huang, Hsing-Hui Su, Yi-Hung Chen, Jinghua T Chang, Shiang-Suo Huang

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

Article in Frontiers in pharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

21 citing papers in PubMed, 42 citations in OpenAlex.

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  12. Bioevaluation ofMolecules (Basel, Switzerland) · 2021
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  18. Deficiency of Interleukin-36 Receptor Protected Cardiomyocytes from Ischemia-Reperfusion Injury in Cardiopulmonary Bypass.Medical science monitor : international medical journal of experimental and clinical research · 2020
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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

7 authors at 5 institutions in 1 country.

Yi-Hsin WangInstitute of Medicine, Chung Shan Medical University, Taichung, Taiwan.
Shun-An LiSuperintendent Office, Yuanli Lee's General Hospital, Lee's Medical Corporation, Miaoli, Taiwan.
Chao-Hsin HuangDepartment of Internal Medicine, Dajia Lee's General Hospital, Lee's Medical Corporation, Taichung, Taiwan.
Hsing-Hui SuDepartment and Institute of Pharmacology, School of Medicine, National Yang-Ming University, Taipei, Taiwan.
Yi-Hung ChenGraduate Institute of Acupuncture Science and Research Center for Chinese Medicine and Acupuncture, China Medical University, Taichung, Taiwan.
Jinghua T ChangInstitute of Medicine, Chung Shan Medical University, Taichung, Taiwan.
Shiang-Suo HuangDepartment of Pharmacology and Institute of Medicine, Chung Shan Medical University, Taichung, Taiwan.
Chung Shan Medical University · TWChina Medical University · TWChung Shan Medical University Hospital · TWNational Yang Ming Chiao Tung University · TWYuan's General Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lumbrokinase is used as an oral supplement to support and maintain healthy cardiovascular function, and to treat cardiovascular diseases in clinical for more than 10 years. Up until now, the mechanism of the cardioprotective effects of post-ischemic treatment with lumbrokinase has remained unclear. We therefore investigated the signaling pathways involved in the amelioration of myocardial ischemia-reperfusion (I-R) injury in rats treated with lumbrokinase 20 min after myocardial ischemia. Compared to vehicle-treated rats, post-ischemic treatment with lumbrokinase was associated with significant reductions in myocardial I-R-induced arrhythmias and myocardial damage, and an improvement in cardiac function. Moreover, lumbrokinase significantly upregulated levels of silent information regulator 1 (Sirt1). In addition, lumbrokinase significantly increased manganese-dependent superoxide dismutase expression, decreased Cleaved-Caspase-3 expression, and induced deacetylation of FoxO1. On the other hand, lumbrokinase also significantly downregulated levels of succinate dehydrogenase, cytochrome c oxidase, nuclear factor kappa B (NF-κB) and elevated levels of microtubule-associated protein light chain 3. Notably, the cardioprotective effects of lumbrokinase were abolished by administration of the specific Sirt1 inhibitor EX527. These findings demonstrate that post-ischemic treatment with lumbrokinase attenuates myocardial I-R injury through the activation of Sirt1 signaling, and thus enhances autophagic flux and reduces I-R-induced oxidative damage, inflammation and apoptosis.

Indexed as

cardioprotectionischemialumbrokinasereperfusionSirt1

Identifiers

PMID29962953
PMCPMC6013847
OpenAlexW2806052998

What OpenQuestion holds

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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.