Evidence map›Paper›PMID 22628574›Full record

ReviewCirculation research2012

Cardiac-specific inducible and conditional gene targeting in mice.

Thomas Doetschman, Mohamad Azhar

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Circulation research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

41 citing papers in PubMed, 1 synthesis or guideline pooled it.

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  20. The Pitfalls ofFrontiers in physiology · 2021
    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

2 authors.

Thomas DoetschmanBIO5 Institute and Department of Cellular & Molecular Medicine, University of Arizona, Tucson, AZ, USA.
Mohamad Azhar

Funding

Roles of FGF2 and TGFbeta in cardiac hypertrophyR01HL070174 · NHLBI · UNIVERSITY OF CINCINNATI · PI DOETSCHMAN, THOMAS · 2002 to 2005
$1.5M
NHLBI NIH HHS R01 HL070174
6 · The paper itself

Abstract

Mouse genetic engineering has revolutionized our understanding of the molecular and genetic basis of heart development and disease. This technology involves conditional tissue-specific and temporal transgenic and gene targeting approaches, as well as introduction of polymorphisms into the mouse genome. These approaches are increasingly used to elucidate the genetic pathways underlying tissue homeostasis, physiology, and pathophysiology of adult heart. They have also led to the development of clinically relevant models of human cardiac diseases. Here, we review the technologies and their limitations in general and the cardiovascular research community in particular.

Indexed as

Gene Expression Regulation, DevelopmentalGene TargetingHeartAlternative SplicingAnimalsDeoxyribonucleasesDisease Models, AnimalEndothelial CellsFibroblastsHeart Conduction SystemHeart DiseasesHumansMiceMice, KnockoutMice, TransgenicMicroRNAsDeoxyribonucleasesMicroRNAs

Identifiers

PMID22628574
PMCPMC3855383

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.