Evidence map›Paper›PMID 34311122›Full record

ArticleBone2021

ACVR1

Koji Matsuo, Abigail Lepinski, Robert D Chavez, Emilie Barruet, Ashley Pereira, Tania A Moody, Amy N Ton, Aditi Sharma, Judith Hellman, Kiichiro Tomoda and 2 more

Erratum issuedOpen access · hybridAbstract read
In one paragraph

Article in Bone, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
5.6field-weighted citation impact, top 3% 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

25 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
  2. Review
  3. Gut microbiome-dependent IL-1 signaling is a mediator of ACVR1bioRxiv : the preprint server for biology · 2026
    Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Matrix metalloproteinase-9 deficiency confers resilience in fibrodysplasia ossificans progressiva in a man and mice.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2024
    Article
  11. Review
  12. Review
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 4 institutions in 1 country.

Koji MatsuoDivision of Endocrinology and Metabolism, Department of Medicine, University of California, San Francisco, CA, USA; The Institute for Human Genetics, University of California, San Francisco, CA, USA; The Program in Craniofacial Biology, University of California, San Francisco, CA, USA.
Abigail LepinskiDivision of Endocrinology and Metabolism, Department of Medicine, University of California, San Francisco, CA, USA; The Institute for Human Genetics, University of California, San Francisco, CA, USA; The Program in Craniofacial Biology, University of California, San Francisco, CA, USA; Division of Graduate Medical Sciences, Boston University School of Medicine, Boston, MA, USA.
Robert D ChavezDivision of Endocrinology and Metabolism, Department of Medicine, University of California, San Francisco, CA, USA; The Institute for Human Genetics, University of California, San Francisco, CA, USA; The Program in Craniofacial Biology, University of California, San Francisco, CA, USA.
Emilie BarruetDivision of Endocrinology and Metabolism, Department of Medicine, University of California, San Francisco, CA, USA; The Institute for Human Genetics, University of California, San Francisco, CA, USA; The Program in Craniofacial Biology, University of California, San Francisco, CA, USA.
Ashley PereiraDivision of Endocrinology and Metabolism, Department of Medicine, University of California, San Francisco, CA, USA; The Institute for Human Genetics, University of California, San Francisco, CA, USA; The Program in Craniofacial Biology, University of California, San Francisco, CA, USA.
Tania A MoodyDivision of Endocrinology and Metabolism, Department of Medicine, University of California, San Francisco, CA, USA; The Institute for Human Genetics, University of California, San Francisco, CA, USA; The Program in Craniofacial Biology, University of California, San Francisco, CA, USA.
Amy N TonDivision of Endocrinology and Metabolism, Department of Medicine, University of California, San Francisco, CA, USA; The Institute for Human Genetics, University of California, San Francisco, CA, USA; The Program in Craniofacial Biology, University of California, San Francisco, CA, USA.
Aditi SharmaDivision of Endocrinology and Metabolism, Department of Medicine, University of California, San Francisco, CA, USA; The Institute for Human Genetics, University of California, San Francisco, CA, USA; The Program in Craniofacial Biology, University of California, San Francisco, CA, USA.
Judith HellmanDepartment of Anesthesia and Perioperative Care, University of California, San Francisco, USA.
Kiichiro TomodaGladstone Institute of Cardiovascular Disease, San Francisco, CA, USA.
Mary C NakamuraMedical Service, San Francisco Veterans Affairs Healthcare System, San Francisco, CA, USA; Department of Medicine, University of California, San Francisco, CA, USA.
Edward C HsiaoDivision of Endocrinology and Metabolism, Department of Medicine, University of California, San Francisco, CA, USA; The Institute for Human Genetics, University of California, San Francisco, CA, USA; The Program in Craniofacial Biology, University of California, San Francisco, CA, USA. Electronic address: Edward.hsiao@ucsf.edu.
University of California, San Francisco · USBoston University · USGladstone Institutes · USSan Francisco VA Medical Center · US

Funding

RESOURCE-BASED CENTER FOR THE ADVANCEMENT OF PRECISION MEDICINE IN RHEUMATOLOGYP30AR070155 · NIAMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI Mary C Nakamura · 2016 to 2026
$8.2M
Skeletal Biology and Biomechanics (SBB) CoreP30AR075055 · NIAMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI EDWARD C HSIAO · 2019 to 2026
$7.1M
Microphysiological systems to interrogate the Islet-Liver-Adipose Axis in normal physiology and Type-2 Diabetes MellitusUH3DK120004 · NIDDK · UNIVERSITY OF CALIFORNIA BERKELEY · PI HEALY, KEVIN EDWARD, HEBROK, MATTHIAS · 2020 to 2022
$6.9M
Training Program in Rheumatic and Musculoskeletal Diseases ResearchT32AR069516 · NIAMS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI John D Mountz · 2016 to 2026
$2.6M
Microphysiological systems to interrogate the Islet-Liver-Adipose Axis in normal physiology and Type-2 Diabetes MellitusUG3DK120004 · NIDDK · UNIVERSITY OF CALIFORNIA BERKELEY · PI HEALY, KEVIN EDWARD, HEBROK, MATTHIAS · 2018 to 2019
$2.3M
Innate immune regulation of stem cells in bone formationR01AR066735 · NIAMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI HSIAO, EDWARD C · 2015 to 2019
$1.8M
Pharmacologic modulation of innate immune dysfunction in heterotopic ossificationR01AR073015 · NIAMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI HSIAO, EDWARD C · 2018 to 2021
$1.4M
Elucidating skeletal stem cell function using engineered 3D multicellular structuresR21AR072778 · NIAMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI HSIAO, EDWARD C · 2018 to 2019
$536k
BLRD VA I01 BX002994NIAMS NIH HHS P30 AR070155NIAMS NIH HHS P30 AR075055NIAMS NIH HHS R01 AR066735NIAMS NIH HHS R01 AR073015NIAMS NIH HHS R21 AR072778NIAMS NIH HHS T32 AR069516NIDDK NIH HHS UG3 DK120004NIDDK NIH HHS UH3 DK120004
6 · The paper itself

Abstract

Macrophages play crucial roles in many human disease processes. However, obtaining large numbers of primary cells for study is often difficult. We describe 2D and 3D methods for directing human induced pluripotent stem cells (hiPSCs) into macrophages (iMACs). iMACs generated in 2D culture showed functional similarities to human primary monocyte-derived M2-like macrophages, and could be successfully polarized into a M1-like phenotype. Both M1- and M2-like iMACs showed phagocytic activity and reactivity to endogenous or exogenous stimuli. In contrast, iMACs generated by a 3D culture system showed mixed M1- and M2-like functional characteristics. 2D-iMACs from patients with fibrodysplasia ossificans progressiva (FOP), an inherited disease with progressive heterotopic ossification driven by inflammation, showed prolonged inflammatory cytokine production and higher Activin A production after M1-like polarization, resulting in dampened responses to additional LPS stimulation. These results demonstrate a simple and robust way of creating hiPSC-derived M1- and M2-like macrophage lineages, while identifying macrophages as a source of Activin A that may drive heterotopic ossification in FOP.

Indexed as

Induced Pluripotent Stem CellsMyositis OssificansOssification, HeterotopicActivin Receptors, Type IHumansMacrophagesSignal TransductionActivin Receptors, Type IACVR1 protein, humanActivin ACytokinesFibrodysplasia ossificans progressivaFOPHeterotopic ossificationHuman induced pluripotent stem cellsImmune activationInflammationMacrophages

Identifiers

PMID34311122
PMCPMC8803261
OpenAlexW3186040648

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.