Evidence map›Paper›PMID 23326427›Full record

ArticlePloS one2013

3,3'-Diindolylmethane protects against cardiac hypertrophy via 5'-adenosine monophosphate-activated protein kinase-α2.

Jing Zong, Wei Deng, Heng Zhou, Zhou-yan Bian, Jia Dai, Yuan Yuan, Jie-yu Zhang, Rui Zhang, Yan Zhang, Qing-qing Wu and 3 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

11 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. DIM attenuates TGF-β1-induced myofibroblast differentiation in neonatal rat cardiac fibroblasts.International journal of clinical and experimental pathology · 2015
    Article
  9. Article
  10. New approaches to radiation protection.Frontiers in oncology · 2014
    Review
  11. 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

13 authors at 3 institutions in 1 country.

Jing ZongDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan, China.
Wei Deng
Heng Zhou
Zhou-yan Bian
Jia Dai
Yuan Yuan
Jie-yu Zhang
Rui Zhang
Yan Zhang
Qing-qing Wu
Hai-peng Guo
Hong-liang Li
Qi-zhu Tang
Wuhan University · CNRenmin Hospital of Wuhan University · CNQilu Hospital of Shandong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purpose3,3'-Diindolylmethane (DIM) is a natural component of cruciferous plants. It has strong antioxidant and anti-angiogenic effects and promotes the apoptosis of a variety of tumor cells. However, little is known about the critical role of DIM on cardiac hypertrophy. In the present study, we investigated the effects of DIM on cardiac hypertrophy.

methodsMultiple molecular techniques such as Western blot analysis, real-time PCR to determine RNA expression levels of hypertrophic, fibrotic and oxidative stress markers, and histological analysis including H&E for histopathology, PSR for collagen deposition, WGA for myocyte cross-sectional area, and immunohistochemical staining for protein expression were used.

resultsIn pre-treatment and reverse experiments, C57/BL6 mouse chow containing 0.05% DIM (dose 100 mg/kg/d DIM) was administered one week prior to surgery or one week after surgery, respectively, and continued for 8 weeks after surgery. In both experiments, DIM reduced to cardiac hypertrophy and fibrosis induced by aortic banding through the activation of 5'-adenosine monophosphate-activated protein kinase-α2 (AMPKα2) and inhibition of mammalian target of the rapamycin (mTOR) signaling pathway. Furthermore, DIM protected against cardiac oxidative stress by regulating expression of estrogen-related receptor-alpha (ERRα) and NRF2 etc. The cardioprotective effects of DIM were ablated in mice lacking functional AMPKα2.

conclusionDIM significantly improves left ventricular function via the activation of AMPKα2 in a murine model of cardiac hypertrophy.

Indexed as

AMP-Activated Protein KinasesAnimalsCardiomegalyCardiotonic AgentsFibrosisIndolesMaleMiceMice, Inbred C57BLMice, KnockoutOxidative StressPhosphorylationRibosomal Protein S6 Kinases, 70-kDaSignal TransductionTOR Serine-Threonine Kinases3,3'-diindolylmethaneAMP-Activated Protein KinasesCardiotonic AgentsIndolesPrkaa2 protein, mouseRibosomal Protein S6 Kinases, 70-kDaTOR Serine-Threonine Kinases

Identifiers

PMID23326427
PMCPMC3541184
OpenAlexW1998550705

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LicenceCC BY
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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.