Evidence map›Paper›PMID 23423573›Full record

ArticleDiabetes2013

A novel mechanism by which SDF-1β protects cardiac cells from palmitate-induced endoplasmic reticulum stress and apoptosis via CXCR7 and AMPK/p38 MAPK-mediated interleukin-6 generation.

Yuguang Zhao, Yi Tan, Shugang Xi, Yunqian Li, Cai Li, Jiuwei Cui, Xiaoqing Yan, Xiaokun Li, Guanjun Wang, Wei Li and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Diabetes, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

20 citing papers in PubMed, 58 citations in OpenAlex.

  1. Article
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  3. Young Sca-1Journal of nanobiotechnology · 2023
    Article
  4. p53 and Myofibroblast Apoptosis in Organ Fibrosis.International journal of molecular sciences · 2023
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. CXCR7 Targeting and Its Major Disease Relevance.Frontiers in pharmacology · 2018
    Review
  10. Article
  11. Article
  12. The Role of p38 MAPK in the Development of Diabetic Cardiomyopathy.International journal of molecular sciences · 2016
    Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Article
  20. 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

11 authors at 5 institutions in 2 countries.

Yuguang ZhaoCancer Center, the First Hospital of Jilin University, Changchun, China.
Yi Tan
Shugang Xi
Yunqian Li
Cai Li
Jiuwei Cui
Xiaoqing Yan
Xiaokun Li
Guanjun Wang
Wei Li
Lu Cai
First Hospital of Jilin University · CNJilin University · CNUniversity of Louisville · USWenzhou Medical University · CNKosair Children's Hospital · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We studied the protective effect of stromal cell-derived factor-1β (SDF-1β) on cardiac cells from lipotoxicity in vitro and diabetes in vivo. Exposure of cardiac cells to palmitate increased apoptosis by activating NADPH oxidase (NOX)-associated nitrosative stress and endoplasmic reticulum (ER) stress, which was abolished by pretreatment with SDF-1β via upregulation of AMP-activated protein kinase (AMPK)-mediated p38 mitogen-activated protein kinase (MAPK) phosphorylation and interleukin-6 (IL-6) production. The SDF-1β cardiac protection could be abolished by inhibition of AMPK, p38 MAPK, or IL-6. Activation of AMPK or addition of recombinant IL-6 recaptured a similar cardiac protection. SDF-1β receptor C-X-C chemokine receptor type 4 (CXCR4) antagonist AMD3100 or CXCR4 small interfering RNA could not, but CXCR7 small interfering RNA completely abolished SDF-1β's protection from palmitate-induced apoptosis and activation of AMPK and p38 MAPK. Administration of SDF-1β to diabetic rats, induced by feeding a high-fat diet, followed by a small dose of streptozotocin, could significantly reduce cardiac apoptosis and increase AMPK phosphorylation along with prevention of diabetes-induced cardiac oxidative damage, inflammation, hypertrophy, and remodeling. These results showed that SDF-1β protects against palmitate-induced cardiac apoptosis, which is mediated by NOX-activated nitrosative damage and ER stress, via CXCR7, to activate AMPK/p38 MAPK-mediated IL-6 generation. The cardiac protection by SDF-1β from diabetes-induced oxidative damage, cell death, and remodeling was also associated with AMPK activation.

Indexed as

Adenylate KinaseAnimalsApoptosisBenzylaminesCell LineChemokine CXCL12CyclamsDiabetes Mellitus, ExperimentalDiet, High-FatEndoplasmic Reticulum StressHeterocyclic CompoundsInterleukin-6MaleNADPH Oxidasesp38 Mitogen-Activated Protein KinasesPalmitic AcidAckr3 protein, ratAdenylate KinaseBenzylaminesChemokine CXCL12Cxcr4 protein, ratCyclamsHeterocyclic CompoundsInterleukin-6NADPH Oxidasesp38 Mitogen-Activated Protein KinasesPalmitic AcidplerixaforReceptors, CXCRReceptors, CXCR4

Identifiers

PMID23423573
PMCPMC3712029
OpenAlexW2157443006

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.