Evidence map›Paper›PMID 32133214›Full record

ArticleBone research2020

Osteoclasts are not a source of SLIT3.

Na Li, Kazuki Inoue, Jun Sun, Yingzhen Niu, Sarfaraz Lalani, Alisha Yallowitz, Xu Yang, Chao Zhang, Rong Shen, Baohong Zhao and 2 more

Open access · goldAbstract read
In one paragraph

Article in Bone research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

32 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
  2. Review
  3. Osteoclast-Derived SLIT3 Mediates Osteoarthritis Pain and Degenerative Changes.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. SLIT3-mediated fibroblast signaling: a promising target for antifibrotic therapies.American journal of physiology. Heart and circulatory physiology · 2023
    Review
  17. Review
  18. Review
  19. Article
  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

12 authors at 3 institutions in 2 countries.

Na Li *1State Key Laboratory of Cellular Stress Biology, School of Medicine, Xiamen University, Xiamen, Fujian China.
Kazuki Inoue *2Arthritis and Tissue Degeneration Program and David Z. Rosensweig Genomics Research Center, Hospital for Special Surgery, New York, NY USA.
Jun Sun4Department of Pathology and Laboratory Medicine, Weill Cornell Medical College, Cornell University, New York, NY USA.
Yingzhen Niu5Division of Adult Reconstruction and Joint Replacement, Department of Orthopedic Surgery, Hospital for Special Surgery, New York, NY USA.
Sarfaraz Lalani4Department of Pathology and Laboratory Medicine, Weill Cornell Medical College, Cornell University, New York, NY USA.
Alisha Yallowitz4Department of Pathology and Laboratory Medicine, Weill Cornell Medical College, Cornell University, New York, NY USA.
Xu Yang5Division of Adult Reconstruction and Joint Replacement, Department of Orthopedic Surgery, Hospital for Special Surgery, New York, NY USA.
Chao Zhang6Institute for Computational Biomedicine, Cornell University, New York, NY USA.
Rong Shen1State Key Laboratory of Cellular Stress Biology, School of Medicine, Xiamen University, Xiamen, Fujian China.
Baohong Zhao2Arthritis and Tissue Degeneration Program and David Z. Rosensweig Genomics Research Center, Hospital for Special Surgery, New York, NY USA.
Ren Xu1State Key Laboratory of Cellular Stress Biology, School of Medicine, Xiamen University, Xiamen, Fujian China.
Matthew B Greenblatt4Department of Pathology and Laboratory Medicine, Weill Cornell Medical College, Cornell University, New York, NY USA.
Cornell University · USHospital for Special Surgery · USXiamen University · CN

Funding

Regulation of Osteoclastogenesis and Arthritic Bone Resorption by RBP-JR01AR071463 · NIAMS · HOSPITAL FOR SPECIAL SURGERY · PI Kyung-Hyun Park-Min · 2017 to 2026
$4.0M
Modulation of Bone Formation by SHN3DP5OD021351 · OD · WEILL MEDICAL COLL OF CORNELL UNIV · PI GREENBLATT, MATTHEW BLAKE · 2015 to 2019
$2.1M
Mechanisms of inflammatory bone remodelingR01AR068970 · NIAMS · HOSPITAL FOR SPECIAL SURGERY · PI ZHAO, BAOHONG · 2016 to 2021
$1.9M
"Establishing Pathways for Endothelial Support of Bone Formation with SLIT3"R01AR075585 · NIAMS · WEILL MEDICAL COLL OF CORNELL UNIV · PI GREENBLATT, MATTHEW BLAKE · 2020 to 2024
$1.8M
NIAMS NIH HHS R01 AR068970NIAMS NIH HHS R01 AR071463NIAMS NIH HHS R01 AR075585NIH HHS DP5 OD021351
6 · The paper itself

Abstract

The axon guidance cue SLIT3 was identified as an osteoanabolic agent in two recent reports. However, these reports conflict in their nomination of osteoblasts versus osteoclasts as the key producers of skeletal SLIT3 and additionally offer conflicting data on the effects of SLIT3 on osteoclastogenesis. Here, aiming to address this discrepancy, we found no observable SLIT3 expression during human or mouse osteoclastogenesis and the only modest SLIT3-mediated effects on osteoclast differentiation. Conditional deletion of SLIT3 in cathepsin K (CTSK)-positive cells, including osteoclasts, had no effect on the number of osteoclast progenitors, in vitro osteoclast differentiation, overall bone mass, or bone resorption/formation parameters. Similar results were observed with the deletion of SLIT3 in LysM-positive cells, including osteoclast lineage cells. Consistent with this finding, bone marrow chimeras made from

Indexed as

BoneMetabolism

Identifiers

PMID32133214
PMCPMC7031526
OpenAlexW3006912887

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.