Evidence map›Paper›PMID 27791458›Full record

ArticleAutophagy2017

Store-operated calcium entry-activated autophagy protects EPC proliferation via the CAMKK2-MTOR pathway in ox-LDL exposure.

Jie Yang, Jie Yu, Dongdong Li, Sanjiu Yu, Jingbin Ke, Lianyou Wang, Yanwei Wang, Youzhu Qiu, Xubin Gao, Jihang Zhang and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Autophagy, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
4.1field-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

48 citing papers in PubMed, 67 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. STIM1 in tumor cell death: angel or devil?Cell death discovery · 2023
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Review
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 2 institutions in 1 country.

Jie Yanga Institute of Cardiovascular Diseases, Xinqiao Hospital, Third Military Medical University , Chongqing , China.
Jie Yua Institute of Cardiovascular Diseases, Xinqiao Hospital, Third Military Medical University , Chongqing , China.
Dongdong Lia Institute of Cardiovascular Diseases, Xinqiao Hospital, Third Military Medical University , Chongqing , China.
Sanjiu Yua Institute of Cardiovascular Diseases, Xinqiao Hospital, Third Military Medical University , Chongqing , China.
Jingbin Kea Institute of Cardiovascular Diseases, Xinqiao Hospital, Third Military Medical University , Chongqing , China.
Lianyou Wanga Institute of Cardiovascular Diseases, Xinqiao Hospital, Third Military Medical University , Chongqing , China.
Yanwei Wanga Institute of Cardiovascular Diseases, Xinqiao Hospital, Third Military Medical University , Chongqing , China.
Youzhu Qiua Institute of Cardiovascular Diseases, Xinqiao Hospital, Third Military Medical University , Chongqing , China.
Xubin Gaoa Institute of Cardiovascular Diseases, Xinqiao Hospital, Third Military Medical University , Chongqing , China.
Jihang Zhanga Institute of Cardiovascular Diseases, Xinqiao Hospital, Third Military Medical University , Chongqing , China.
Lan Huanga Institute of Cardiovascular Diseases, Xinqiao Hospital, Third Military Medical University , Chongqing , China.
Army Medical University · CNXinqiao Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Improving biological functions of endothelial progenitor cells (EPCs) is beneficial to maintaining endothelium homeostasis and promoting vascular re-endothelialization. Because macroautophagy/autophagy has been documented as a double-edged sword in cell functions, its effects on EPCs remain to be elucidated. This study was designed to explore the role and molecular mechanisms of store-operated calcium entry (SOCE)-activated autophagy in proliferation of EPCs under hypercholesterolemia. We employed oxidized low-density lipoprotein (ox-LDL) to mimic hypercholesterolemia in bone marrow-derived EPCs from rat. Ox-LDL dose-dependently activated autophagy flux, while inhibiting EPC proliferation. Importantly, inhibition of autophagy either by silencing Atg7 or by 3-methyladenine treatment, further aggravated proliferative inhibition by ox-LDL, suggesting the protective effects of autophagy against ox-LDL. Interestingly, ox-LDL increased STIM1 expression and intracellular Ca

Indexed as

AnimalsAutophagyCalciumCalcium-Calmodulin-Dependent Protein Kinase KinaseCalcium ChannelsCell ProliferationChelating AgentsEndothelial CellsGene SilencingGreen Fluorescent ProteinsHumansHypercholesterolemiaLipoproteins, LDLMalePhosphorylationRatsCalciumCalcium-Calmodulin-Dependent Protein Kinase KinaseCalcium ChannelsCamkk2 protein, ratChelating AgentsGreen Fluorescent ProteinsLipoproteins, LDLoxidized low density lipoproteinTOR Serine-Threonine KinasesautophagyCAMKK2cell-based therapyendothelial progenitor cellsMTORoxidized low-density lipoproteinproliferationstore-operated calcium entry

Identifiers

PMID27791458
PMCPMC5240837
OpenAlexW2543352617

What OpenQuestion holds

Textmetadata
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.