Evidence map›Paper›PMID 25118288›Full record

Trial reportThe Journal of biological chemistry2014

Shock wave treatment enhances cell proliferation and improves wound healing by ATP release-coupled extracellular signal-regulated kinase (ERK) activation.

Anna M Weihs, Christiane Fuchs, Andreas H Teuschl, Joachim Hartinger, Paul Slezak, Rainer Mittermayr, Heinz Redl, Wolfgang G Junger, Harald H Sitte, Dominik Rünzler

Open access · hybridAbstract readClinical Trial
In one paragraph

Trial report in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
87citing papers in PubMed, 3 pooled it
7.9field-weighted citation impact, top 2% 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

87 citing papers in PubMed, 3 syntheses or guidelines pooled it, 166 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Trial
  5. Trial
  6. Trial
  7. Review
  8. Review
  9. Extracorporeal shockwave therapy in tissue repair and regeneration.Wiener medizinische Wochenschrift (1946) · 2026
    Review
  10. Article
  11. Article
  12. Review
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  14. Review
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  16. Tendinopathy: The Interplay between Mechanical Stress, Inflammation, and Vascularity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Review
  17. Article
  18. Review
  19. Article
  20. Article

27 more citing papers are in PubMed but not listed here.

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

10 authors at 5 institutions in 2 countries.

Anna M WeihsDepartment of Biochemical Engineering, University of Applied Sciences Technikum Wien, 1200 Vienna, Austria,; The Austrian Cluster for Tissue Regeneration, Vienna, Austria.
Christiane FuchsDepartment of Biochemical Engineering, University of Applied Sciences Technikum Wien, 1200 Vienna, Austria,; The Austrian Cluster for Tissue Regeneration, Vienna, Austria,. Electronic address: fuchsc@technikum-wien.at.
Andreas H TeuschlDepartment of Biochemical Engineering, University of Applied Sciences Technikum Wien, 1200 Vienna, Austria,; The Austrian Cluster for Tissue Regeneration, Vienna, Austria.
Joachim HartingerThe Austrian Cluster for Tissue Regeneration, Vienna, Austria,; Ludwig Boltzmann Institute for Experimental and Clinical Traumatology/Austrian Workers' Compensation Board (AUVA) Research Center, 1200 Vienna, Austria.
Paul SlezakThe Austrian Cluster for Tissue Regeneration, Vienna, Austria,; Ludwig Boltzmann Institute for Experimental and Clinical Traumatology/Austrian Workers' Compensation Board (AUVA) Research Center, 1200 Vienna, Austria.
Rainer MittermayrThe Austrian Cluster for Tissue Regeneration, Vienna, Austria,; Ludwig Boltzmann Institute for Experimental and Clinical Traumatology/Austrian Workers' Compensation Board (AUVA) Research Center, 1200 Vienna, Austria.
Heinz RedlThe Austrian Cluster for Tissue Regeneration, Vienna, Austria,; Ludwig Boltzmann Institute for Experimental and Clinical Traumatology/Austrian Workers' Compensation Board (AUVA) Research Center, 1200 Vienna, Austria.
Wolfgang G JungerLudwig Boltzmann Institute for Experimental and Clinical Traumatology/Austrian Workers' Compensation Board (AUVA) Research Center, 1200 Vienna, Austria,; Department of Surgery, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215, and.
Harald H SitteInstitute of Pharmacology, Center for Physiology and Pharmacology, Medical University of Vienna, 1090 Vienna, Austria.
Dominik RünzlerDepartment of Biochemical Engineering, University of Applied Sciences Technikum Wien, 1200 Vienna, Austria,; The Austrian Cluster for Tissue Regeneration, Vienna, Austria.
University of Applied Sciences Technikum Wien · ATLudwig Boltzmann Institute for Experimental and Clinical Traumatology · ATAustrian Cluster for Tissue Regeneration · ATBeth Israel Deaconess Medical Center · USMedical University of Vienna · AT

Funding

Neutrophil activation and traumaR01GM060475 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI JUNGER, WOLFGANG G · 2001 to 2016
$3.8M
Purinergic regulation of T cellsR01GM051477 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI JUNGER, WOLFGANG G · 2003 to 2016
$2.5M
NIGMS NIH HHS R01 GM051477NIGMS NIH HHS R01 GM060475
6 · The paper itself

Abstract

Shock wave treatment accelerates impaired wound healing in diverse clinical situations. However, the mechanisms underlying the beneficial effects of shock waves have not yet been fully revealed. Because cell proliferation is a major requirement in the wound healing cascade, we used in vitro studies and an in vivo wound healing model to study whether shock wave treatment influences proliferation by altering major extracellular factors and signaling pathways involved in cell proliferation. We identified extracellular ATP, released in an energy- and pulse number-dependent manner, as a trigger of the biological effects of shock wave treatment. Shock wave treatment induced ATP release, increased Erk1/2 and p38 MAPK activation, and enhanced proliferation in three different cell types (C3H10T1/2 murine mesenchymal progenitor cells, primary human adipose tissue-derived stem cells, and a human Jurkat T cell line) in vitro. Purinergic signaling-induced Erk1/2 activation was found to be essential for this proliferative effect, which was further confirmed by in vivo studies in a rat wound healing model where shock wave treatment induced proliferation and increased wound healing in an Erk1/2-dependent fashion. In summary, this report demonstrates that shock wave treatment triggers release of cellular ATP, which subsequently activates purinergic receptors and finally enhances proliferation in vitro and in vivo via downstream Erk1/2 signaling. In conclusion, our findings shed further light on the molecular mechanisms by which shock wave treatment exerts its beneficial effects. These findings could help to improve the clinical use of shock wave treatment for wound healing.

Indexed as

Cell ProliferationHigh-Energy Shock WavesMAP Kinase Signaling SystemWound HealingAdenosine TriphosphateAdultAnimalsEnzyme ActivationExtracellular Signal-Regulated MAP KinasesFemaleHumansJurkat CellsMaleMiceRatsRats, Sprague-DawleyAdenosine TriphosphateExtracellular Signal-Regulated MAP KinasesATPCell ProliferationExtracellular Signal-regulated Kinase (ERK)Shock Wave TreatmentSignal TransductionWound Healing

Identifiers

PMID25118288
PMCPMC4175346
OpenAlexW2089324929

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.