Evidence map›Paper›PMID 30103389›Full record

ReviewInternational journal of molecular sciences2018

TGF-Beta Signaling in Bone with Chronic Kidney Disease.

Yoshiko Iwasaki, Hideyuki Yamato, Masafumi Fukagawa

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.6field-weighted citation impact, top 33% 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

13 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. TGFβ signaling regulates the response of the skeleton to phosphate.bioRxiv : the preprint server for biology · 2025
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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

3 authors at 2 institutions in 1 country.

Yoshiko IwasakiDepartment of Health Sciences, Oita University of Nursing and Health Sciences, Oita 870-1163, Japan. iwasaki@oita-nhs.ac.jp.
Hideyuki YamatoDivision of Nephrology and Metabolism, Tokai University School of Medicine, Kanagawa 259-119, Japan. hyamato0602@yahoo.co.jp.
Masafumi FukagawaDivision of Nephrology and Metabolism, Tokai University School of Medicine, Kanagawa 259-119, Japan. fukagawa@tokai-u.jp.
Tokai University · JPOita University of Nursing and Health Sciences · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transforming growth factor (TGF)-β signaling is not only important in skeletal development, but also essential in bone remodeling in adult bone. The bone remodeling process involves integrated cell activities induced by multiple stimuli to balance bone resorption and bone formation. TGF-β plays a role in bone remodeling by coordinating cell activities to maintain bone homeostasis. However, mineral metabolism disturbance in chronic kidney disease (CKD) results in abnormal bone remodeling, which leads to ectopic calcification in CKD. High circulating levels of humoral factors such as parathyroid hormone, fibroblast growth factor 23, and Wnt inhibitors modulate bone remodeling in CKD. Several reports have revealed that TGF-β is involved in the production and functions of these factors in bone. TGF-β may act as a factor that mediates abnormal bone remodeling in CKD.

Indexed as

Bone RemodelingWnt Signaling PathwayAnimalsBone and BonesFibroblast Growth Factor-23Fibroblast Growth FactorsHumansRenal Insufficiency, ChronicTransforming Growth Factor betaFibroblast Growth Factor-23Fibroblast Growth FactorsTransforming Growth Factor betabone remodelingchronic kidney diseasehumoral factorsmineral metabolism disturbance

Identifiers

PMID30103389
PMCPMC6121599
OpenAlexW2885160791

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.