Evidence map›Paper›PMID 33614650›Full record

ReviewFrontiers in cell and developmental biology2021

Monocyte/Macrophage Lineage Cells From Fetal Erythromyeloid Progenitors Orchestrate Bone Remodeling and Repair.

Yasuhito Yahara, Xinyi Ma, Liam Gracia, Benjamin A Alman

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in cell and developmental biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

26 citing papers in PubMed, 43 citations in OpenAlex.

  1. Review
  2. Article
  3. Developmental Pathways of Immature CD11cInternational journal of molecular sciences · 2026
    Review
  4. What's New in Musculoskeletal Basic Science.The Journal of bone and joint surgery. American volume · 2025
    Article
  5. Review
  6. Review
  7. Review
  8. Review
  9. Article
  10. Distinct cross talk of IL-17 & TGF-β with the immature CD11cImmunity, inflammation and disease · 2024
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. 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

4 authors at 1 institution in 2 countries.

Yasuhito YaharaDepartment of Orthopaedic Surgery, Duke University School of Medicine, Durham, NC, United States.
Xinyi MaDepartment of Orthopaedic Surgery, Duke University School of Medicine, Durham, NC, United States.
Liam GraciaDepartment of Orthopaedic Surgery, Duke University School of Medicine, Durham, NC, United States.
Benjamin A AlmanDepartment of Orthopaedic Surgery, Duke University School of Medicine, Durham, NC, United States.
Duke University · US

Funding

Training Program in Developmental & Stem Cell BiologyT32HD040372 · NICHD · DUKE UNIVERSITY · PI Terry H Lechler · 2001 to 2026
$8.9M
The role of macrophage subpopulations in the rejuvenation of fracture repairR01AG072058 · NIA · DUKE UNIVERSITY · PI ALMAN, BENJAMIN AARON · 2021 to 2025
$2.1M
Rejuvenating fracture repair: The role of the macrophage and Beta-cateninR01AG049745 · NIA · DUKE UNIVERSITY · PI ALMAN, BENJAMIN AARON · 2016 to 2020
$1.9M
NIA NIH HHS R01 AG049745NIA NIH HHS R01 AG072058NICHD NIH HHS T32 HD040372
6 · The paper itself

Abstract

A third of the population sustains a bone fracture, and the pace of fracture healing slows with age. The slower pace of repair is responsible for the increased morbidity in older individuals who sustain a fracture. Bone healing progresses through overlapping phases, initiated by cells of the monocyte/macrophage lineage. The repair process ends with remodeling. This last phase is controlled by osteoclasts, which are bone-specific multinucleated cells also of the monocyte/macrophage lineage. The slower rate of healing in aging can be rejuvenated by macrophages from young animals, and secreted proteins from macrophage regulate undifferentiated mesenchymal cells to become bone-forming osteoblasts. Macrophages can derive from fetal erythromyeloid progenitors or from adult hematopoietic progenitors. Recent studies show that fetal erythromyeloid progenitors are responsible for the osteoclasts that form the space in bone for hematopoiesis and the fetal osteoclast precursors reside in the spleen postnatally, traveling through the blood to participate in fracture repair. Differences in secreted proteins between macrophages from old and young animals regulate the efficiency of osteoblast differentiation from undifferentiated mesenchymal precursor cells. Interestingly, during the remodeling phase osteoclasts can form from the fusion between monocyte/macrophage lineage cells from the fetal and postnatal precursor populations. Data from single cell RNA sequencing identifies specific markers for populations derived from the different precursor populations, a finding that can be used in future studies. Here, we review the diversity of macrophages and osteoclasts, and discuss recent finding about their developmental origin and functions, which provides novel insights into their roles in bone homeostasis and repair.

Indexed as

erythromyeloid progenitorsfracturemacrophageosteoclastremodelingyolk sac

Identifiers

PMID33614650
PMCPMC7889961
OpenAlexW3128337426

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.