Evidence map›Paper›PMID 38267638›Full record

ReviewCell research2024

The roles and regulatory mechanisms of TGF-β and BMP signaling in bone and cartilage development, homeostasis and disease.

Mengrui Wu, Shali Wu, Wei Chen, Yi-Ping Li

Open access · hybridAbstract readReview
In one paragraph

Review in Cell research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 253 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
253citing papers in PubMed, 2 pooled it
76.2field-weighted citation impact, top 1% 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

253 citing papers in PubMed, 2 syntheses or guidelines pooled it, 326 citations in OpenAlex.

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193 more citing papers are in PubMed but not listed here.

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 2 institutions in 2 countries.

Mengrui WuDepartment of Cell and Developmental Biology, College of Life Sciences, Zhejiang University, Hangzhou, Zhejiang, China. mengruiwu@zju.edu.cn.
Shali WuDepartment of Cell and Developmental Biology, College of Life Sciences, Zhejiang University, Hangzhou, Zhejiang, China.
Wei ChenDivision in Cellular and Molecular Medicine, Department of Pathology and Laboratory Medicine, Tulane University School of Medicine, Tulane University, New Orleans, LA, USA.
Yi-Ping LiDivision in Cellular and Molecular Medicine, Department of Pathology and Laboratory Medicine, Tulane University School of Medicine, Tulane University, New Orleans, LA, USA. yli81@tulane.edu.ORCID 0000-0003-2188-6958
Tulane University · USZhejiang University · CN

Funding

Inhibiting Periodontitis by Targeting Cathepsin K and Attenuating TLR SignalingR01DE023813 · NIDCR · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI LI, YI-PING · 2014 to 2023
$3.9M
Mechanistic basis of the role of Cbx3 in negatively regulating osteoclast differentiation through epigenetic modificationR01AR075735 · NIAMS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI LI, YI-PING · 2019 to 2024
$2.4M
Cbfβ mediates articular cartilage regeneration and repair in agingR01AG056438 · NIA · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI CHEN, WEI · 2019 to 2023
$2.1M
Gα13 signaling attenuates periodontal inflammation and alveolar bone loss in the mouse model of age-associated periodontitisR01DE028264 · NIDCR · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI LI, YI-PING · 2018 to 2022
$1.8M
Characterizing the negative signaling in dendritic cells and macrophages to attenuate inflammation and bone destruction in Rheumatoid arthritisR01AR074954 · NIAMS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI LI, YI-PING · 2020 to 2024
$1.6M
Characterizing the mechanism by which endogenous negative regulators of osteoclasts control bone homeostasis under physiological and pathological conditions in mouse modelsR01AR070135 · NIAMS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI CHEN, WEI · 2017 to 2021
$1.6M
Cbfβ mediates articular cartilage regeneration and repair in agingR56AG056438 · NIA · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI CHEN, WEI · 2017 to 2017
$371k
NIAMS NIH HHS R01 AR070135NIAMS NIH HHS R01 AR074954NIAMS NIH HHS R01 AR075735NIA NIH HHS R01 AG056438NIA NIH HHS R56 AG056438NIDCR NIH HHS R01 DE023813NIDCR NIH HHS R01 DE028264
6 · The paper itself

Abstract

Transforming growth factor-βs (TGF-βs) and bone morphometric proteins (BMPs) belong to the TGF-β superfamily and perform essential functions during osteoblast and chondrocyte lineage commitment and differentiation, skeletal development, and homeostasis. TGF-βs and BMPs transduce signals through SMAD-dependent and -independent pathways; specifically, they recruit different receptor heterotetramers and R-Smad complexes, resulting in unique biological readouts. BMPs promote osteogenesis, osteoclastogenesis, and chondrogenesis at all differentiation stages, while TGF-βs play different roles in a stage-dependent manner. BMPs and TGF-β have opposite functions in articular cartilage homeostasis. Moreover, TGF-β has a specific role in maintaining the osteocyte network. The precise activation of BMP and TGF-β signaling requires regulatory machinery at multiple levels, including latency control in the matrix, extracellular antagonists, ubiquitination and phosphorylation in the cytoplasm, nucleus-cytoplasm transportation, and transcriptional co-regulation in the nuclei. This review weaves the background information with the latest advances in the signaling facilitated by TGF-βs and BMPs, and the advanced understanding of their diverse physiological functions and regulations. This review also summarizes the human diseases and mouse models associated with disordered TGF-β and BMP signaling. A more precise understanding of the BMP and TGF-β signaling could facilitate the development of bona fide clinical applications in treating bone and cartilage disorders.

Indexed as

Bone Morphogenetic ProteinsChondrogenesisTransforming Growth Factor betaAnimalsBone and BonesCartilageHomeostasisHumansMiceBone Morphogenetic ProteinsTransforming Growth Factor beta

Identifiers

PMID38267638
PMCPMC10837209
OpenAlexW4391168196

What OpenQuestion holds

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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.