Evidence map›Paper›PMID 37898628›Full record

ArticleCell death & disease2023

Loss of adenosine A3 receptors accelerates skeletal muscle regeneration in mice following cardiotoxin-induced injury.

Nastaran Tarban, Albert Bálint Papp, Dávid Deák, Péter Szentesi, Hajnalka Halász, Andreas Patsalos, László Csernoch, Zsolt Sarang, Zsuzsa Szondy

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

4 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. CD47 Promotes, While Exposure to Apoptotic Cells Destroys the Fusion Program of Differentiating Myoblasts.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
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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

9 authors at 2 institutions in 2 countries.

Nastaran Tarban *Doctoral School of Molecular Cell and Immune Biology, University of Debrecen, Debrecen, Hungary.
Albert Bálint Papp *Doctoral School of Dental Sciences, University of Debrecen, Debrecen, Hungary.
Dávid DeákLaboratory Animal Facility, Life Science Building, University of Debrecen, Debrecen, Hungary.
Péter SzentesiDepartment of Physiology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Hajnalka HalászDoctoral School of Molecular Cell and Immune Biology, University of Debrecen, Debrecen, Hungary.
Andreas PatsalosDepartments of Medicine and Biological Chemistry, Johns Hopkins University School of Medicine, Institute for Fundamental Biomedical Research, Johns Hopkins All Children's Hospital, St, Petersburg, FL, USA.ORCID 0000-0002-9022-4985
László CsernochDepartment of Physiology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Zsolt SarangDepartment of Biochemistry and Molecular Biology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Zsuzsa SzondyDepartment of Biochemistry and Molecular Biology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary. szondy@med.unideb.hu.ORCID 0000-0001-8347-9552
University of Debrecen · HUJohns Hopkins University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Skeletal muscle regeneration is a complex process orchestrated by multiple interacting steps. An increasing number of reports indicate that inflammatory responses play a central role in linking initial muscle injury responses to timely muscle regeneration following injury. The nucleoside adenosine has been known for a long time as an endogenously produced anti-inflammatory molecule that is generated in high amounts during tissue injury. It mediates its physiological effects via four types of adenosine receptors. From these, adenosine A3 receptors (A3Rs) are not expressed by the skeletal muscle but are present on the surface of various inflammatory cells. In the present paper, the effect of the loss of A3Rs was investigated on the regeneration of the tibialis anterior (TA) muscle in mice following cardiotoxin-induced injury. Here we report that regeneration of the skeletal muscle from A3R

Indexed as

CardiotoxinsMuscle, SkeletalReceptor, Adenosine A3Satellite Cells, Skeletal MuscleAnimalsMiceMuscle Fibers, SkeletalCardiotoxinsReceptor, Adenosine A3

Identifiers

PMID37898628
PMCPMC10613231
OpenAlexW4388000287

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.