Evidence map›Paper›PMID 34518518›Full record

ArticleBone research2021

Epo/EpoR signaling in osteoprogenitor cells is essential for bone homeostasis and Epo-induced bone loss.

Martina Rauner, Marta Murray, Sylvia Thiele, Deepika Watts, Drorit Neumann, Yankel Gabet, Lorenz C Hofbauer, Ben Wielockx

Open access · goldAbstract read
In one paragraph

Article in Bone research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

23 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Article
  3. Interferon-JAK-STAT Axis in Bone Metabolism.Current osteoporosis reports · 2026
    Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Pharmacological inhibition of HIF2 protects against bone loss in an experimental model of estrogen deficiency.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  10. Article
  11. Loss ofGenes · 2024
    Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Erythropoietin and Skeletal Cells CrossTalks in Physiology and Disease.Current opinion in endocrine and metabolic research · 2023
    Article
  17. Article
  18. Article
  19. Review
  20. 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

8 authors at 2 institutions in 2 countries.

Martina RaunerDepartment of Medicine III & Center for Healthy Aging, Technische Universität Dresden, Dresden, Germany. martina.rauner@ukdd.de.
Marta MurrayInstitute for Clinical Chemistry and Laboratory Medicine, Technische Universität Dresden, Dresden, Germany.
Sylvia ThieleDepartment of Medicine III & Center for Healthy Aging, Technische Universität Dresden, Dresden, Germany.
Deepika WattsInstitute for Clinical Chemistry and Laboratory Medicine, Technische Universität Dresden, Dresden, Germany.
Drorit NeumannDepartment of Cell and Developmental Biology, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel.
Yankel GabetDepartment of Anatomy & Anthropology, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel.
Lorenz C HofbauerDepartment of Medicine III & Center for Healthy Aging, Technische Universität Dresden, Dresden, Germany.
Ben WielockxInstitute for Clinical Chemistry and Laboratory Medicine, Technische Universität Dresden, Dresden, Germany. ben.wielockx@tu-dresden.de.ORCID http://orcid.org/0000-0002-4923-2596
Technische Universität Dresden · DETel Aviv University · IL

Funding

German-Israeli Foundation for Scientific Research and Development (GIF) #I-1433-203.13_2017
6 · The paper itself

Abstract

High erythropoietin (Epo) levels are detrimental to bone health in adult organisms. Adult mice receiving high doses of Epo lose bone mass due to suppressed bone formation and increased bone resorption. In humans, high serum Epo levels are linked to fractures in elderly men. Our earlier studies indicated that Epo modulates osteoblast activity; however, direct evidence that Epo acts via its receptor (EpoR) on osteoblasts in vivo is still missing. Here, we created mice lacking EpoR in osteoprogenitor cells to specifically address this gap. Deletion of EpoR in osteoprogenitors (EpoR:Osx-cre, cKO) starting at 5 weeks of age did not alter red blood cell parameters but increased vertebral bone volume by 25% in 12-week-old female mice. This was associated with low bone turnover. Histological (osteoblast number, bone formation rate) and serum (P1NP, osteocalcin) bone formation parameters were all reduced, as were the number of osteoclasts and TRAP serum level. Differentiation of osteoblast precursors isolated from cKO versus control mice resulted in lower expression of osteoblast marker genes including Runx2, Alp, and Col1a1 on day 21, whereas the mineralization capacity was similar. Moreover, the RANKL/OPG ratio, which determines the osteoclast-supporting potential of osteoblasts, was substantially decreased by 50%. Similarly, coculturing cKO osteoblasts with control or cKO osteoclast precursors produced significantly fewer osteoclasts than coculture with control osteoblasts. Finally, exposing female mice to Epo pumps (10 U·d

Identifiers

PMID34518518
PMCPMC8437981
OpenAlexW3199789276

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.