Evidence map›Paper›PMID 24486907›Full record

ArticleFEBS letters2014

Induction of microRNA-138 by pro-inflammatory cytokines causes endothelial cell dysfunction.

Anagha Sen, Patrick Most, Karsten Peppel

Abstract read
In one paragraph

Article in FEBS letters, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
3.0field-weighted citation impact, top 8% 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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 40 citations in OpenAlex.

  1. Pooled it
  2. The Role of miR-138 in Cardiovascular Diseases.BioMed research international · 2025
    Review
  3. miRNAs in Heart Development and Disease.International journal of molecular sciences · 2024
    Review
  4. Article
  5. Article
  6. Article
  7. Observational
  8. Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Regulatory miRNAs in Colorectal Carcinogenesis and Metastasis.International journal of molecular sciences · 2017
    Review
  15. Article
  16. Article
  17. Article
  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

3 authors at 2 institutions in 2 countries.

Anagha SenCenter for Translational Medicine, Jefferson Medical College, Philadelphia, PA, USA.
Patrick MostCenter for Translational Medicine, Jefferson Medical College, Philadelphia, PA, USA; Laboratory for Molecular and Translational Cardiology, Department of Internal Medicine III, University of Heidelberg, INF 350, 69120 Heidelberg, Germany; DZHK (German Center for Cardiovascular Research), Partner site Heidelberg/Mannheim, Heidelberg University Hospital, INF 410, 69120 Heidelberg, Germany.
Karsten PeppelCenter for Translational Medicine, Jefferson Medical College, Philadelphia, PA, USA. Electronic address: Karsten.Peppel@Jefferson.edu.
Jefferson College · USHeidelberg University · DE

Funding

S100A1: A Novel Modulator of Myocardial Infarct Inflammation and RegenerationR01HL092130 · NHLBI · THOMAS JEFFERSON UNIVERSITY · PI PEPPEL, KARSTEN · 2008 to 2012
$2.2M
Inflammation in Vein Graft Disease: A Genetic ApproachR01HL072842 · NHLBI · THOMAS JEFFERSON UNIVERSITY · PI PEPPEL, KARSTEN · 2004 to 2007
$1.5M
NHLBI NIH HHS HL 092130-02S1NHLBI NIH HHS R01 HL 072842NHLBI NIH HHS R01 HL072842NHLBI NIH HHS R01 HL092130NHLBI NIH HHS R01 HL 092130-01
6 · The paper itself

Abstract

Exposure to pro-inflammatory cytokines, such as Angiotensin II, endothelin-1 or TNF leads to endothelial dysfunction, characterized by the reduced production of nitric oxide via endothelial nitric oxide synthase (eNOS). We recently identified the Ca(2+) binding protein S100A1 as an essential factor required for eNOS activity. Here we report that pro-inflammatory cytokines down-regulate expression of S100A1 in primary human microvascular endothelial cells (HMVECs) via induction of microRNA-138 (miR-138), in a manner that depends on the stabilization of HIF1-α. We show that loss of S100A1 in ECs reduces stimulus-induced NO production, which can be prevented by inhibition of miR-138. Our study suggests that targeting miR-138 might be beneficial for the treatment of cardiovascular disease.

Indexed as

Transcriptional ActivationAngiotensin IICardiovascular DiseasesCell LineEndothelial CellsEndothelin-1HumansHypoxia-Inducible Factor 1, alpha SubunitInflammation MediatorsMAP Kinase Signaling SystemMicroRNAsMitogen-Activated Protein KinasesNitric Oxide Synthase Type IIIPhosphorylationProtein Processing, Post-TranslationalS100 ProteinsAngiotensin IIEndothelin-1HIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitInflammation MediatorsMicroRNAsMIRN138 microRNA, humanMitogen-Activated Protein KinasesNitric Oxide Synthase Type IIINOS3 protein, humanS100A1 proteinS100 ProteinsTumor Necrosis Factor-alphaAngiotensin IICytokineEndothelial dysfunctionEndothelial nitric oxide synthaseEndothelin-1Tumor necrosis factor-alpha

Identifiers

PMID24486907
PMCPMC3975049
OpenAlexW1971335899

What OpenQuestion holds

Textmetadata
LicenceTDM
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.