Evidence map›Paper›PMID 26989860›Full record

ArticleJournal of cellular and molecular medicine2016

Effects of short-chain acyl-CoA dehydrogenase on cardiomyocyte apoptosis.

Zhenhua Zeng, Qiuju Huang, Zhaohui Shu, Peiqing Liu, Shaorui Chen, Xuediao Pan, Linquan Zang, Sigui Zhou

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

Article in Journal of cellular and molecular medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
1.2field-weighted citation impact, top 23% 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

2 citing papers in PubMed, 16 citations in OpenAlex.

  1. Review
  2. Article
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

8 authors at 2 institutions in 1 country.

Zhenhua ZengDepartment of Clinical Pharmacy, GuangDong Pharmaceutical University, Guangzhou, China.
Qiuju HuangDepartment of Clinical Pharmacy, GuangDong Pharmaceutical University, Guangzhou, China.
Zhaohui ShuDepartment of Clinical Pharmacy, GuangDong Pharmaceutical University, Guangzhou, China.
Peiqing LiuDepartment of Pharmacology and Toxicology, School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou, China.
Shaorui ChenDepartment of Pharmacology and Toxicology, School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou, China.
Xuediao PanDepartment of Clinical Pharmacy, GuangDong Pharmaceutical University, Guangzhou, China.
Linquan ZangDepartment of Clinical Pharmacy, GuangDong Pharmaceutical University, Guangzhou, China.
Sigui ZhouDepartment of Clinical Pharmacy, GuangDong Pharmaceutical University, Guangzhou, China.
Guangdong Pharmaceutical University · CNSun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Short-chain acyl-CoA dehydrogenase (SCAD), a key enzyme of fatty acid β-oxidation, plays an important role in cardiac hypertrophy. However, its effect on the cardiomyocyte apoptosis remains unknown. We aimed to determine the role of SCAD in tert-butyl hydroperoxide (tBHP)-induced cardiomyocyte apoptosis. The mRNA and protein expression of SCAD were significantly down-regulated in the cardiomyocyte apoptosis model. Inhibition of SCAD with siRNA-1186 significantly decreased SCAD expression, enzyme activity and ATP content, but obviously increased the content of free fatty acids. Meanwhile, SCAD siRNA treatment triggered the same apoptosis as cardiomyocytes treated with tBHP, such as the increase in cell apoptotic rate, the activation of caspase3 and the decrease in the Bcl-2/Bax ratio, which showed that SCAD may play an important role in primary cardiomyocyte apoptosis. The changes of phosphonate AMP-activated protein kinase α (p-AMPKα) and Peroxisome proliferator-activated receptor α (PPARα) in cardiomyocyte apoptosis were consistent with that of SCAD. Furthermore, PPARα activator fenofibrate and AMPKα activator AICAR treatment significantly increased the expression of SCAD and inhibited cardiomyocyte apoptosis. In conclusion, for the first time our findings directly demonstrated that SCAD may be as a new target to prevent cardiomyocyte apoptosis through the AMPK/PPARα/SCAD signal pathways.

Indexed as

ApoptosisAminoimidazole CarboxamideAMP-Activated Protein KinasesAnimalsAnimals, NewbornButyryl-CoA DehydrogenaseCardiotonic AgentsCell DeathCell SurvivalFenofibrateMyocytes, CardiacPPAR alphaRats, Sprague-DawleyReal-Time Polymerase Chain ReactionRibonucleotidesRNA, Small InterferingAICA ribonucleotideAminoimidazole CarboxamideAMP-Activated Protein KinasesButyryl-CoA DehydrogenaseCardiotonic AgentsFenofibratePPAR alphaRibonucleotidesRNA, Small Interferingtert-ButylhydroperoxideAMP-activated protein kinasecardiomyocyte apoptosisenergy metabolism•peroxisome proliferator-activated receptor αshort-chain acyl-CoA dehydrogenasetert-butyl hydroperoxide

Identifiers

PMID26989860
PMCPMC4929297
OpenAlexW2298069123

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.