Evidence map›Paper›PMID 25986681›Full record

ReviewMedical molecular morphology2015

Double heterozygous mice for Klf5 and Fli1 genes: a new animal model of systemic sclerosis recapitulating its three cardinal pathological features.

Yoshihide Asano

Abstract readReview
PubMed Publisher
In one paragraph

Review in Medical molecular morphology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.7field-weighted citation impact, top 31% 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

1 citing paper in PubMed, 7 citations in OpenAlex.

  1. Article
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

1 author at 1 institution in 1 country.

Yoshihide AsanoDepartment of Dermatology, University of Tokyo Graduate School of Medicine, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-8655, Japan. yasano-tky@umin.ac.jp.
The University of Tokyo · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The lack of animal models recapitulating the three cardinal features of systemic sclerosis (SSc), such as immune activation, vasculopathy, and tissue fibrosis, hinders the understanding of the pathogenesis of this disease. A series of clinical studies has suggested that environmental factors largely contribute to the development of SSc in individuals predisposed by genetic factors. This notion is supported by the establishment of a new murine SSc model which recapitulates three cardinal features of SSc by simultaneous haploinsufficiency of Klf5 and Fli1 genes, both of which are epigenetically suppressed in SSc dermal fibroblasts. In addition to enhanced dermal thickness, Klf5(+/-) and Fli1(+/-) mice resemble dermal fibrosis of SSc at the ultrastructural level. Furthermore, these mice simulate altered vascular structure and B cell activation characteristic of SSc. Further studies on the pathological events in Klf5(+/-) and Fli1(+/-) mice and the roles of KLF5 and Fli1 in various types of cells may provide us with a useful clue to better understand the developmental process of SSc.

Indexed as

Disease Models, AnimalAnimalsFibroblastsHeterozygoteKruppel-Like Transcription FactorsMiceProto-Oncogene Protein c-fli-1Scleroderma, SystemicFli1 protein, mouseKlf5 protein, mouseKruppel-Like Transcription FactorsProto-Oncogene Protein c-fli-1EpigeneticsFli1KLF5Systemic sclerosisUltrastructure of collagen fibrils

Identifiers

PMID25986681
OpenAlexW329440530

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.