Evidence map›Paper›PMID 26887388›Full record

ReviewJournal of molecular endocrinology2016

Regulation of liver development: implications for liver biology across the lifespan.

Philip A Gruppuso, Jennifer A Sanders

Open access · bronzeAbstract readReview
In one paragraph

Review in Journal of molecular endocrinology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
10.5field-weighted citation impact, top 2% 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

29 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.

  1. Pooled it
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  14. Silibinin Schiff Base Derivatives Counteract CClDrug design, development and 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 1 country.

Philip A GruppusoDivision of Pediatric EndocrinologyRhode Island Hospital and Brown University, Providence, RI, USA Department of Molecular BiologyCell Biology and Biochemistry, Brown University, Providence, RI, USA Philip_Gruppuso@brown.edu.
Jennifer A SandersDivision of Pediatric EndocrinologyRhode Island Hospital and Brown University, Providence, RI, USA Department of Pathology and Laboratory MedicineBrown University, Providence, RI, USA.
Brown University · USRhode Island Hospital · US

Funding

REGULATION OF FETAL HEPATIC GROWTHR01HD024455 · NICHD · RHODE ISLAND HOSPITAL (PROVIDENCE, RI) · PI GRUPPUSO, PHILIP A. · 1989 to 2022
$7.9M
The Fetal Hepatocyte Phenotype and Cell-Based Therapy for Liver DiseaseR01DK100301 · NIDDK · RHODE ISLAND HOSPITAL · PI GRUPPUSO, PHILIP A., SANDERS, JENNIFER A · 2014 to 2017
$1.4M
NICHD NIH HHS R01 HD024455NIDDK NIH HHS R01 DK100301
6 · The paper itself

Abstract

The liver serves a spectrum of essential metabolic and synthetic functions that are required for the transition from fetal to postnatal life. Processes essential to the attainment of adequate liver mass and function during fetal life include cell lineage specification early in development, enzymic and other functional modes of differentiation throughout gestation, and ongoing cell proliferation to achieve adequate liver mass. Available data in laboratory rodents indicate that the signaling networks governing these processes in the fetus differ from those that can sustain liver function and mass in the adult. More specifically, fetal hepatocytes may develop independent of key mitogenic signaling pathways, including those involving the Erk mitogen-activated protein kinases MAPK1/3 and the mechanistic target of rapamycin (mTOR). In addition, the fetal liver is subject to environmental influences that, through epigenetic mechanisms, can have sustained effects on function and, by extension, contribute to the developmental origin of adult metabolic disease. Finally, the mitogen-independent phenotype of rat fetal hepatocytes in late gestation makes these cells suitable for cell-based therapy of liver injury. In the aggregate, studies on the mechanisms governing fetal liver development have implications not only for the perinatal metabolic transition but also for the prevention and treatment of liver disorders throughout the lifespan.

Indexed as

OrganogenesisAnimalsCell- and Tissue-Based TherapyCell DifferentiationCell LineageFemaleGene Expression Regulation, DevelopmentalHepatocytesHumansInsulinIntercellular Signaling Peptides and ProteinsLiverLiver DiseasesMaternal Nutritional Physiological PhenomenaPhenotypePrimatesInsulinIntercellular Signaling Peptides and Proteinsdevelopmentepigeneticsgrowth factorsinsulin actionmetabolism

Identifiers

PMID26887388
PMCPMC4882189
OpenAlexW2292763365

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.