Evidence map›Paper›PMID 33620678›Full record

ArticleCardiovascular drugs and therapy2022

The Protective Role of Bmal1-Regulated Autophagy Mediated by HDAC3/SIRT1 Pathway in Myocardial Ischemia/Reperfusion Injury of Diabetic Rats.

Zhen Qiu, Hao Ming, Yi Zhang, Yanli Yu, Shaoqing Lei, Zhong-Yuan Xia

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Article in Cardiovascular drugs and therapy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.0field-weighted citation impact, top 28% 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

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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

14 citing papers in PubMed, 12 citations in OpenAlex.

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  14. Bee venom ameliorates cardiac dysfunction in diabetic hyperlipidemic rats.Experimental biology and medicine (Maywood, N.J.) · 2021
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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

6 authors at 1 institution in 1 country.

Zhen QiuDepartment of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan, 430060, Hubei, China.
Hao MingDepartment of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan, 430060, Hubei, China.
Yi ZhangDepartment of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan, 430060, Hubei, China.
Yanli YuDepartment of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan, 430060, Hubei, China.
Shaoqing LeiDepartment of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan, 430060, Hubei, China. leishaoqing@163.com.
Zhong-Yuan XiaDepartment of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan, 430060, Hubei, China. xiazhongyuan2005@aliyun.com.
Wuhan University · CN

Funding

the National Natural Science Foundation of China 81970722 and 81671891
6 · The paper itself

Abstract

purposeHistone deacetylase 3 (HDAC3) and silent information regulator 1 (SIRT1) are histone deacetylases that regulate important metabolic pathways and play important roles in diabetes and myocardial ischemia/reperfusion (IR) injury. In this study, we explored the protective mechanism of Bmal1-regulated autophagy mediated by the HDAC3/SIRT1 pathway in myocardial IR injury of diabetic rats. METHODS AND

resultsType 1 diabetes was established by administering an intraperitoneal injection of streptozotocin. After 8 weeks, the left anterior descending coronary artery was ligated for 30 min and reperfused for 120 min to establish a myocardial IR injury model in diabetic rats. H9c2 cardiomyocytes were exposed to high glucose concentration (30 mM) and hypoxia/reoxygenation (H/R) stimulation in vitro. The myocardial infarct size and levels of serum cTn-I, CK-MB, and LDH in diabetic rats subjected to myocardial IR injury were significantly higher. Upregulated HDAC3 and downregulated SIRT1 expression were observed in diabetic and IR hearts, along with a lower Bmal1 level. Autophagy was rapidly increased in the hearts of diabetic or non-diabetic rats in the IR group compared with the sham group, but significantly attenuated in the hearts of diabetic rats compared with the hearts of non-diabetic rats after IR insult. Consistent with decreased autophagy, we observed increased HDAC3 expression and decreased SIRT1 and Bmal1 levels in the myocardial tissue of diabetic rats after IR. Inhibition of HDAC3 by the inhibitor RGFP966 and activation of SIRT1 by the agonist SRT1720 could significantly attenuate myocardial IR injury in diabetic rats by restoring Bmal1-regulated autophagy.

conclusionBased on these findings, the disordered HDAC3/SIRT1 circuit (upregulated HDAC3 and downregulated SIRT1 levels) plays an important role in aggravating myocardial IR injury in diabetic rats by downregulating Bmal1-mediated autophagy. Treatments targeting HDAC3/SIRT1 to activate the autophagy may represent a novel strategy to alleviate myocardial IR injury in diabetes.

Indexed as

Diabetes Mellitus, ExperimentalMyocardial Reperfusion InjuryAnimalsApoptosisARNTL Transcription FactorsAutophagyHistone Deacetylase 3Histone DeacetylasesMyocytes, CardiacOxidative StressRatsSirtuin 1Arntl protein, ratARNTL Transcription FactorsHistone Deacetylase 3Histone DeacetylasesSirt1 protein, ratSirtuin 1AutophagyBmal1HDAC3Myocardial ischemia reperfusion injurySIRT1

Identifiers

PMID33620678
OpenAlexW3129894754

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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.