Evidence map›Paper›PMID 33603953›Full record

ArticleOxidative medicine and cellular longevity2021

Baicalin Improves Cardiac Outcome and Survival by Suppressing Drp1-Mediated Mitochondrial Fission after Cardiac Arrest-Induced Myocardial Damage.

Jun Wu, Hui Chen, Jiahong Qin, Nan Chen, Shiqi Lu, Jun Jin, Yi Li

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

Article in Oxidative medicine and cellular longevity, 2021. 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
2.0field-weighted citation impact, top 13% 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, 35 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

7 authors at 4 institutions in 1 country.

Jun WuDepartment of Ultrasonography Medicine, Suzhou Hospital of Traditional Chinese Medicine, 215009 Suzhou, China.
Hui ChenDepartment of Emergency Medicine, Traditional Chinese Medicine Hospital of Kunshan, 215300 Kunshan, China.
Jiahong QinDepartment of Intensive Care Unit, The First Affiliated Hospital of Kunming Medical University, 650032 Kunming, China.
Nan ChenDepartment of Intensive Care Unit, The First Affiliated Hospital of Soochow University, 215006 Suzhou, China.
Shiqi LuDepartment of Intensive Care Unit, The First Affiliated Hospital of Soochow University, 215006 Suzhou, China.
Jun JinDepartment of Intensive Care Unit, The First Affiliated Hospital of Soochow University, 215006 Suzhou, China.
Yi LiDepartment of Intensive Care Unit, The First Affiliated Hospital of Soochow University, 215006 Suzhou, China.ORCID https://orcid.org/0000-0001-7995-9385
Soochow University · CNKunming Medical University · CNShanghai University of Traditional Chinese Medicine · CNSuzhou Research Institute · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myocardial injury after cardiac arrest (CA) often results in severe myocardial dysfunction and death involving mitochondrial dysfunction. Here, we sought to investigate whether baicalin, a natural flavonoid compound, exerts cardioprotection against CA-induced injury via regulating mitochondrial dysfunction. We subjected the rats to asphyxia CA after a daily baicalin treatment for 4 weeks. After the return of spontaneous circulation, baicalin treatment significantly improved cardiac function performance, elevated survival rate from 35% to 75%, prevented necrosis and apoptosis in the myocardium, which was accompanied by reduced phosphorylation of Drp1 at serine 616, inhibited Drp1 translocation to the mitochondria and mitochondrial fission, and improved mitochondrial function. In H9c2 cells subjected to simulated ischemia/reperfusion, increased phosphorylation of Drp1 at serine 616 and subsequently enhanced mitochondrial Drp1 translocation as well as mitochondrial fission, augmented cardiomyocyte death, increased reactive oxygen species production, released cytochrome c from mitochondria and injured mitochondrial respiration were efficiently improved by baicalin and Drp1 specific inhibitor with Mdivi-1. Furthermore, overexpression of Drp1 augmented excessive mitochondrial fission and abolished baicalin-afforded cardioprotection, indicating that the protective impacts of baicalin are linked to the inhibition of Drp1. Altogether, our findings disclose for the first time that baicalin offers cardioprotection against ischemic myocardial injury after CA by inhibiting Drp1-mediated mitochondrial fission. Baicalin might be a prospective therapy for the treatment of post-CA myocardial injury.

Indexed as

Mitochondrial DynamicsAnimalsCell LineCell RespirationCytochromes cDynaminsFlavonoidsHeart ArrestHemodynamicsMaleMitochondriaMyocardiumRatsRats, Sprague-DawleyReactive Oxygen SpeciesReturn of Spontaneous CirculationbaicalinCytochromes cDnm1l protein, ratDynaminsFlavonoidsReactive Oxygen Species

Identifiers

PMID33603953
PMCPMC7870315
OpenAlexW3129084572

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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.