Evidence map›Paper›PMID 20698835›Full record

ArticleAging cell2010

Decreased oxidative stress and greater bone anabolism in the aged, when compared to the young, murine skeleton with parathyroid hormone administration.

Robert L Jilka, Maria Almeida, Elena Ambrogini, Li Han, Paula K Roberson, Robert S Weinstein, Starros C Manolagas

Open access · greenAbstract readComparative Study
In one paragraph

Article in Aging cell, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed
4.9field-weighted citation impact, top 4% 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

71 citing papers in PubMed, 124 citations in OpenAlex.

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  10. Autophagy: regulating the seesaw of bone-fat balance.Frontiers in cell and developmental biology · 2025
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11 more citing papers are in PubMed but not listed here.

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

7 authors at 1 institution in 1 country.

Robert L JilkaCenter for Osteoporosis and Metabolic Bone Diseases, University of Arkansas for Medical Sciences, Little Rock, 72205, USA. rljilka@uams.edu
Maria Almeida
Elena Ambrogini
Li Han
Paula K Roberson
Robert S Weinstein
Starros C Manolagas
University of Arkansas for Medical Sciences · US

Funding

TRANSGENIC MOUSE COREP01AG013918 · NIA · UNIV OF ARKANSAS FOR MED SCIS · PI WEINSTEIN, ROBERT STEWART · 1996 to 2016
$25.7M
NIA NIH HHS P01 AG013918
6 · The paper itself

Abstract

Because of recent insights into the pathogenesis of age-related bone loss, we investigated whether intermittent parathyroid hormone (PTH) administration antagonizes the molecular mechanisms of the adverse effects of aging on bone. Parathyroid hormone produced a greater increase in vertebral trabecular bone mineral density and bone volume as well as a greater expansion of the endocortical bone surface in the femur of 26- when compared to 6 -month-old female C57BL/6 mice. Moreover, PTH increased trabecular connectivity in vertebrae, and the toughness of both vertebrae and femora in old, but not young, mice. Parathyroid hormone also increased the rate of bone formation and reduced osteoblast apoptosis to a greater extent in the old mice. Most strikingly, PTH reduced reactive oxygen species, p66(Shc) phosphorylation, and expression of the lipoxygenase Alox15, and it increased glutathione and stimulated Wnt signaling in bone of old mice. Parathyroid hormone also antagonized the effects of oxidative stress on p66(Shc) phosphorylation, Forkhead Box O transcriptional activity, osteoblast apoptosis, and Wnt signaling in vitro. In contrast, administration of the antioxidants N-acetyl cysteine or pegylated catalase reduced osteoblast progenitors and attenuated proliferation and Wnt signaling. These results suggest that PTH has a greater bone anabolic efficacy in old age because in addition to its other positive actions on bone formation, it antagonizes the age-associated increase in oxidative stress and its adverse effects on the birth and survival of osteoblasts. On the other hand, ordinary antioxidants cannot restore bone mass in old age because they slow remodeling and attenuate osteoblastogenesis by interfering with Wnt signaling.

Indexed as

AgingAnimalsAntioxidantsApoptosisArachidonate 12-LipoxygenaseArachidonate 15-LipoxygenaseBone and BonesBone DensityCell ProliferationCells, CulturedFemaleMiceMice, Inbred C57BLMultienzyme ComplexesOsteoblastsOxidative StressAlox15 protein, mouseAntioxidantsArachidonate 12-LipoxygenaseArachidonate 15-LipoxygenaseMultienzyme ComplexesParathyroid HormoneReactive Oxygen SpeciesShc1 protein, mouseShc Signaling Adaptor ProteinsSrc Homology 2 Domain-Containing, Transforming Protein 1Wnt Proteins

Identifiers

PMID20698835
PMCPMC2958819
OpenAlexW1495319102

What OpenQuestion holds

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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.