Evidence map›Paper›PMID 28523343›Full record

ReviewCellular and molecular life sciences : CMLS2017

Hh signaling in regeneration of the ischemic heart.

Marina Dunaeva, Johannes Waltenberger

Open access · hybridAbstract readReview
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

24 citing papers in PubMed, 43 citations in OpenAlex.

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  14. Signaling pathways and targeted therapy for myocardial infarction.Signal transduction and targeted therapy · 2022
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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

2 authors at 2 institutions in 2 countries.

Marina DunaevaDepartment of Biomolecular Chemistry, Institute for Molecules and Materials and Radboud Institute for Molecular Life Sciences, Radboud University Nijmegen, Nijmegen, The Netherlands.
Johannes WaltenbergerChair of Internal Medicine, Cardiology and Vascular Medicine, Division of Cardiology, Department of Cardiovascular Medicine, University Hospital Münster, Albert-Schweitzer, Campus 1, Building A1, 48149, Münster, Germany. Waltenberger@ukmuenster.de.ORCID 0000-0002-2417-9880
Radboud University Nijmegen · NLUniversity of Münster · DE

Funding

Cells-in-Motion Cluster of Excellence EXC 1003-CiMGerman Research Council SFB656C12
6 · The paper itself

Abstract

Myocardial infarction (MI) is caused by the occlusion of a coronary artery due to underlying atherosclerosis complicated by localized thrombosis. The blockage of blood flow leads to cardiomyocyte (CM) death in the infarcted area. Adult mammalian cardiomyocytes have little capacity to proliferate in response to injury; however, some pathways active during embryogenesis and silent during adult life are recruited in response to tissue injury. One such example is hedgehog (Hh) signaling. Hh is involved in the embryonic development of the heart and coronary vascular system. Pathological conditions including ischemia activate Hh signaling in adult tissues. This review highlights the involvement of Hh signaling in ischemic tissue regeneration with a particular emphasis on heart regeneration and discusses its potential role as a therapeutic agent.

Indexed as

RegenerationSignal TransductionAnimalsCell- and Tissue-Based TherapyCellular Reprogramming TechniquesDrug DiscoveryHeartHedgehog ProteinsHumansMolecular Targeted TherapyMyocardial IschemiaMyocytes, CardiacHedgehog ProteinsCardiomyocytesHeart regenerationHedgehogNeovascularization

Identifiers

PMID28523343
PMCPMC5589787
OpenAlexW2614186512

What OpenQuestion 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 OpenQuestion graph.