Evidence map›Paper›PMID 31800971›Full record

ArticleJournal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research2020

Increased Expression of FGF-21 Negatively Affects Bone Homeostasis in Dystrophin/Utrophin Double Knockout Mice.

Hongshuai Li, Hui Sun, Baoli Qian, Wei Feng, Dwayne Carney, Jennifer Miller, MaCalus V Hogan, Ling Wang

Open access · bronzeAbstract read
In one paragraph

Article in Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

20 citing papers in PubMed, 35 citations in OpenAlex.

  1. Review
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  6. Bone and muscle crosstalk in ageing and disease.Nature reviews. Endocrinology · 2025
    Review
  7. Article
  8. Bone-muscle crosstalk under physiological and pathological conditions.Cellular and molecular life sciences : CMLS · 2024
    Review
  9. International journal of biological sciences · 2024
    Article
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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 1 institution in 2 countries.

Hongshuai LiMusculoskeletal Growth & Regeneration Laboratory, Department of Orthopaedic Surgery, University of Pittsburgh, Pittsburgh, PA, USA.ORCID 0000-0002-9793-0540
Hui SunMusculoskeletal Growth & Regeneration Laboratory, Department of Orthopaedic Surgery, University of Pittsburgh, Pittsburgh, PA, USA.
Baoli QianMusculoskeletal Growth & Regeneration Laboratory, Department of Orthopaedic Surgery, University of Pittsburgh, Pittsburgh, PA, USA.
Wei FengMusculoskeletal Growth & Regeneration Laboratory, Department of Orthopaedic Surgery, University of Pittsburgh, Pittsburgh, PA, USA.
Dwayne CarneyMusculoskeletal Growth & Regeneration Laboratory, Department of Orthopaedic Surgery, University of Pittsburgh, Pittsburgh, PA, USA.
Jennifer MillerMusculoskeletal Growth & Regeneration Laboratory, Department of Orthopaedic Surgery, University of Pittsburgh, Pittsburgh, PA, USA.
MaCalus V HoganMusculoskeletal Growth & Regeneration Laboratory, Department of Orthopaedic Surgery, University of Pittsburgh, Pittsburgh, PA, USA.
Ling WangVascular Medicine Institute, Department of Medicine, University of Pittsburgh, Pittsburgh, PA, USA.
University of Pittsburgh · US

Funding

Targeting Nitrate-Nitrite-NO pathway for Ameliorating Muscle and Bone Comorbidities in Duchenne Muscular DystrophyR01AR076357 · NIAMS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI LI, HONGSHUAI · 2020 to 2024
$1.6M
NIAMS NIH HHS R01 AR076357
6 · The paper itself

Abstract

Duchenne muscular dystrophy (DMD) is the most common muscular dystrophy seen in children. In addition to skeletal muscle, DMD also has a significant impact on bone. The pathogenesis of bone abnormalities in DMD is still unknown. Recently, we have identified a novel bone-regulating cytokine, fibroblast growth factor-21 (FGF-21), which is dramatically upregulated in skeletal muscles from DMD animal models. We hypothesize that muscle-derived FGF-21 negatively affects bone homeostasis in DMD. Dystrophin/utrophin double-knockout (dKO) mice were used in this study. We found that the levels of circulating FGF-21 were significantly higher in dKO mice than in age-matched WT controls. Further tests on FGF-21 expressing tissues revealed that both FGF-21 mRNA and protein expression were dramatically upregulated in dystrophic skeletal muscles, whereas FGF-21 mRNA expression was downregulated in liver and white adipose tissue (WAT) compared to WT controls. Neutralization of circulating FGF-21 by i.p. injection of anti-FGF-21 antibody significantly alleviated progressive bone loss in weight-bearing (vertebra, femur, and tibia) and non-weight bearing bones (parietal bones) in dKO mice. We also found that FGF-21 directly promoted RANKL-induced osteoclastogenesis from bone marrow macrophages (BMMs), as well as promoted adipogenesis while concomitantly inhibiting osteogenesis of bone marrow mesenchymal stem cells (BMMSCs). Furthermore, fibroblast growth factor receptors (FGFRs) and co-receptor β-klotho (KLB) were expressed in bone cells (BMM-derived osteoclasts and BMMSCs) and bone tissues. KLB knockdown by small interfering RNAs (siRNAs) significantly inhibited the effects of FGF21 on osteoclast formation of BMMs and on adipogenic differentiation of BMMSCs, indicating that FGF-21 may directly affect dystrophic bone via the FGFRs-β-klotho complex. In conclusion, this study shows that dystrophic skeletal muscles express and secrete significant levels of FGF-21, which negatively regulates bone homeostasis and represents an important pathological factor for the development of bone abnormalities in DMD. The current study highlights the importance of muscle/bone cross-talk via muscle-derived factors (myokines) in the pathogenesis of bone abnormalities in DMD. © 2019 American Society for Bone and Mineral Research.

Indexed as

DystrophinMuscular Dystrophy, DuchenneAnimalsBone and BonesDisease Models, AnimalFibroblast Growth FactorsHomeostasisMiceMice, Inbred mdxMice, KnockoutMuscle, SkeletalUtrophinDystrophinfibroblast growth factor 21Fibroblast Growth FactorsUtrophinBETA-KLOTHOBONE MARROW MESENCHYMAL STEM CELLS (BMMSCS)DUCHENNE MUSCULAR DYSTROPHY (DMD)FIBROBLAST GROWTH FACTOR-21 (FGF-21)MUSCLE-BONE INTERACTIONSMYOKINESOSTEOCLASTSOSTEOPOROSISSARCOPENIA

Identifiers

PMID31800971
PMCPMC12879057
OpenAlexW2993093494

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.