Evidence map›Paper›PMID 38234849›Full record

ArticleResearch square2024

Long non-coding RNA Malat1 fine-tunes bone homeostasis and repair by orchestrating cellular crosstalk and the β-catenin-OPG/Jagged1 pathway.

Yongli Qin, Jumpei Shirakawa, Cheng Xu, Ruge Chen, Xu Yang, Courtney Ng, Shinichi Nakano, Mahmoud Elguindy, Zhonghao Deng, Kannanganattu V Prasanth and 4 more

Open access · greenAbstract readPreprint
In one paragraph

Article in Research square, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed, 1 citations in OpenAlex.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 3 institutions in 4 countries.

Yongli QinArthritis and Tissue Degeneration Program and David Z. Rosensweig Genomics Research Center, Hospital for Special Surgery, New York, New York, USA.
Jumpei ShirakawaArthritis and Tissue Degeneration Program and David Z. Rosensweig Genomics Research Center, Hospital for Special Surgery, New York, New York, USA.
Cheng XuArthritis and Tissue Degeneration Program and David Z. Rosensweig Genomics Research Center, Hospital for Special Surgery, New York, New York, USA.
Ruge ChenArthritis and Tissue Degeneration Program and David Z. Rosensweig Genomics Research Center, Hospital for Special Surgery, New York, New York, USA.
Xu YangResearch Institute, Hospital for Special Surgery, New York, New York, USA.
Courtney NgArthritis and Tissue Degeneration Program and David Z. Rosensweig Genomics Research Center, Hospital for Special Surgery, New York, New York, USA.
Shinichi NakanoArthritis and Tissue Degeneration Program and David Z. Rosensweig Genomics Research Center, Hospital for Special Surgery, New York, New York, USA.
Mahmoud ElguindyArthritis and Tissue Degeneration Program and David Z. Rosensweig Genomics Research Center, Hospital for Special Surgery, New York, New York, USA.
Zhonghao DengArthritis and Tissue Degeneration Program and David Z. Rosensweig Genomics Research Center, Hospital for Special Surgery, New York, New York, USA.
Kannanganattu V PrasanthDepartment of Cell and Developmental Biology, Cancer center at Illinois, University of Illinois at Urbana-Champaign, Urbana, IL, USA.
Moritz F EissmannInstitute for Tumor Biology and Experimental Therapy, Paul-Ehrlich-Strasse 42-44, 60596 Frankfurt, Germany.
Shinichi NakagawaRNA Biology Laboratory, Faculty of Pharmaceutical Sciences, Hokkaido University, Sapporo 060-0812, Japan.ORCID 0000-0002-6806-7493
William M RicciOrthopaedic Trauma Service, Hospital for Special Surgery & NewYork-Presbyterian Hospital, USA.
Baohong ZhaoArthritis and Tissue Degeneration Program and David Z. Rosensweig Genomics Research Center, Hospital for Special Surgery, New York, New York, USA.
Hospital for Special Surgery · USHokkaido University · JPPaul Ehrlich Institut · DE

Funding

Regulation of Osteoclastogenesis and Arthritic Bone Resorption by RBP-JR01AR071463 · NIAMS · HOSPITAL FOR SPECIAL SURGERY · PI Baohong Zhao · 2017 to 2026
$4.0M
Regulation of bone homeostasis and remodeling by long noncoding RNA Malat1R01AR078212 · NIAMS · HOSPITAL FOR SPECIAL SURGERY · PI Baohong Zhao · 2021 to 2026
$2.2M
Characterization of nuclear-retained RNA-mediated gene regulatory mechanismsR01GM132458 · NIGMS · UNIVERSITY OF ILLINOIS AT URBANA-CHAMPAIGN · PI KANNANGANATTU, PRASANTH KUMAR VIJAYAN · 2020 to 2023
$1.4M
Monoalleleic autosomal spreading of a novel family of nucleolus-localized ncRNAsR21AG065748 · NIA · UNIVERSITY OF ILLINOIS AT URBANA-CHAMPAIGN · PI KANNANGANATTU, PRASANTH KUMAR VIJAYAN · 2020 to 2021
$423k
NIAMS NIH HHS R01 AR071463NIAMS NIH HHS R01 AR078212NIA NIH HHS R21 AG065748NIGMS NIH HHS R01 GM132458
6 · The paper itself

Abstract

The IncRNA Malat1 was initially believed to be dispensable for physiology due to the lack of observable phenotypes in Malat1 knockout (KO) mice. However, our study challenges this conclusion. We found that both Malat1 KO and conditional KO mice in the osteoblast lineage exhibit significant osteoporosis. Mechanistically, Malat1 acts as an intrinsic regulator in osteoblasts to promote osteogenesis. Interestingly, Malat1 does not directly affect osteoclastogenesis but inhibits osteoclastogenesis in a non-autonomous manner

Indexed as

bonefracturehomeostasislncRNAlong non-coding RNAMalat1remodeling

Identifiers

PMID38234849
PMCPMC10793491
OpenAlexW4390346196

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.