Evidence map›Paper›PMID 24471788›Full record

ArticleBritish journal of pharmacology2014

Salidroside exerts angiogenic and cytoprotective effects on human bone marrow-derived endothelial progenitor cells via Akt/mTOR/p70S6K and MAPK signalling pathways.

Yubo Tang, Corina Vater, Angela Jacobi, Cornelia Liebers, Xuenong Zou, Maik Stiehler

Open access · bronzeAbstract read
In one paragraph

Article in British journal of pharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

42 citing papers in PubMed, 65 citations in OpenAlex.

  1. Article
  2. Review
  3. Drug repurposing for cancer therapy.Signal transduction and targeted therapy · 2024
    Review
  4. Article
  5. Review
  6. Article
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  14. Article
  15. Article
  16. Review
  17. Antioxidant Effects of Salidroside in the Cardiovascular System.Evidence-based complementary and alternative medicine : eCAM · 2020
    Review
  18. Article
  19. Protective Effects of Salidroside against Carbon Tetrachloride (CClInternational journal of molecular sciences · 2019
    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

6 authors at 3 institutions in 2 countries.

Yubo TangCentre for Translational Bone, Joint and Soft Tissue Research, Medical Faculty and University Centre for Orthopaedics and Trauma Surgery, University Hospital Carl Gustav Carus at Technische Universität Dresden, Dresden, Germany; Department of Pharmacy, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Corina Vater
Angela Jacobi
Cornelia Liebers
Xuenong Zou
Maik Stiehler
University Hospital Carl Gustav Carus · DETU Dresden · DESun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background and purposeWith the increase of age, increased susceptibility to apoptosis and senescence may contribute to proliferative and functional impairment of endothelial progenitor cells (EPCs). The aim of this study was to investigate whether salidroside (SAL) can induce angiogenic differentiation and inhibit oxidative stress-induced apoptosis in bone marrow-derived EPCs (BM-EPCs), and if so, through what mechanism. EXPERIMENTAL APPROACH: BM-EPCs were isolated and treated with different concentrations of SAL for up to 4 days. Cell proliferation, migration and tube formation ability were detected by DNA content quantification, transwell assay and Matrigel-based angiogenesis assay. Gene and protein expression were assessed by qRT-PCR and Western blot respectively. KEY

resultsTreatment with SAL promoted cellular proliferation and angiogenic differentiation of BM-EPCs, and increased VEGF and NO secretion, which in turn mediated the enhanced angiogenic differentiation of BM-EPCs. Furthermore, SAL significantly attenuated hydrogen peroxide (H₂O₂)-induced cell apoptosis, reduced the intracellular level of reactive oxygen species and restored the mitochondrial membrane potential of BM-EPCs. Moreover, SAL stimulated the phosphorylation of Akt, mammalian target of rapamycin and p70 S6 kinase, as well as ERK1/2, which is associated with cell migration and capillary tube formation. Additionally, SAL reversed the phosphorylation of JNK and p38 MAPK induced by H₂O₂ and suppressed the changes in the Bax/Bcl-xL ratio observed after stimulation with H₂O₂. CONCLUSIONS AND IMPLICATIONS: These findings identify novel mechanisms that regulate EPC function and suggest that SAL has therapeutic potential as a new agent to enhance vasculogenesis as well as protect against oxidative endothelial injury.

Indexed as

AdultAngiogenesis Inducing AgentsBone Marrow CellsCells, CulturedCytoprotectionEndothelial Progenitor CellsGlucosidesHumansMAP Kinase Signaling SystemMiddle AgedPhenolsProto-Oncogene Proteins c-aktRibosomal Protein S6 Kinases, 70-kDaTOR Serine-Threonine KinasesYoung AdultAngiogenesis Inducing AgentsGlucosidesMTOR protein, humanPhenolsProto-Oncogene Proteins c-aktrhodiolosideRibosomal Protein S6 Kinases, 70-kDaTOR Serine-Threonine KinasesAkt/mTOR/p70S6Kangiogenesisapoptosisendothelial progenitor cellMAPKreactive oxygen speciessalidroside

Identifiers

PMID24471788
PMCPMC3997282
OpenAlexW1598095893

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.