Evidence map›Paper›PMID 40308192›Full record

ArticleMolecular therapy : the journal of the American Society of Gene Therapy2025

The p53-miR17 family-Rankl axis bridges liver-bone communication.

Guixing Ma, Siyuan Cheng, Yingying Han, Wanze Tang, Wei Pang, Litong Chen, Zhen Ding, Huiling Cao

Abstract read
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Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

  1. Review
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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.

Guixing MaDepartment of Biochemistry, School of Medicine, Southern University of Science and Technology, Guangdong Provincial Key Laboratory of Cell Microenvironment and Disease Research, Shenzhen Key Laboratory of Cell Microenvironment, Key University Laboratory of Metabolism and Health of Guangdong, Southern University of Science and Technology, Shenzhen 518055, China.
Siyuan ChengDepartment of Biochemistry, School of Medicine, Southern University of Science and Technology, Guangdong Provincial Key Laboratory of Cell Microenvironment and Disease Research, Shenzhen Key Laboratory of Cell Microenvironment, Key University Laboratory of Metabolism and Health of Guangdong, Southern University of Science and Technology, Shenzhen 518055, China.
Yingying HanDepartment of Biochemistry, School of Medicine, Southern University of Science and Technology, Guangdong Provincial Key Laboratory of Cell Microenvironment and Disease Research, Shenzhen Key Laboratory of Cell Microenvironment, Key University Laboratory of Metabolism and Health of Guangdong, Southern University of Science and Technology, Shenzhen 518055, China.
Wanze TangDepartment of Biochemistry, School of Medicine, Southern University of Science and Technology, Guangdong Provincial Key Laboratory of Cell Microenvironment and Disease Research, Shenzhen Key Laboratory of Cell Microenvironment, Key University Laboratory of Metabolism and Health of Guangdong, Southern University of Science and Technology, Shenzhen 518055, China.
Wei PangDepartment of Biochemistry, School of Medicine, Southern University of Science and Technology, Guangdong Provincial Key Laboratory of Cell Microenvironment and Disease Research, Shenzhen Key Laboratory of Cell Microenvironment, Key University Laboratory of Metabolism and Health of Guangdong, Southern University of Science and Technology, Shenzhen 518055, China.
Litong ChenDepartment of Biochemistry, School of Medicine, Southern University of Science and Technology, Guangdong Provincial Key Laboratory of Cell Microenvironment and Disease Research, Shenzhen Key Laboratory of Cell Microenvironment, Key University Laboratory of Metabolism and Health of Guangdong, Southern University of Science and Technology, Shenzhen 518055, China.
Zhen DingDepartment of Biochemistry, School of Medicine, Southern University of Science and Technology, Guangdong Provincial Key Laboratory of Cell Microenvironment and Disease Research, Shenzhen Key Laboratory of Cell Microenvironment, Key University Laboratory of Metabolism and Health of Guangdong, Southern University of Science and Technology, Shenzhen 518055, China.
Huiling CaoDepartment of Biochemistry, School of Medicine, Southern University of Science and Technology, Guangdong Provincial Key Laboratory of Cell Microenvironment and Disease Research, Shenzhen Key Laboratory of Cell Microenvironment, Key University Laboratory of Metabolism and Health of Guangdong, Southern University of Science and Technology, Shenzhen 518055, China. Electronic address: caohl@sustech.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Our study elucidates the crucial role of the liver in bone homeostasis through the p53-miR17 family (miR17-miR20/miR20-miR106/miR93-miR106)-Rankl axis. We demonstrate the enhanced hepatocyte Rankl expression in inflammaging conditions, such as aging, ovariectomized (OVX) mice, and elderly humans. Mice with hepatocyte-specific Rankl deletion exhibit significant resistance to bone mass loss associated with aging, lipopolysaccharide (LPS)-induced inflammation, or estrogen deficiency, compared with controls. Our study highlights hepatocytes as the primary source of Rankl in the liver and serum under these conditions. We identify the p53-miR17 family axis as a crucial regulator for hepatocyte Rankl expression, with p53 inhibiting the miR17 family transcription. Through bioinformatics analysis and in vitro validation, we identify Rankl mRNA as a direct target of the miR17 family. Targeting this axis via CasRx-mediated mRNA editing or miRNA interference significantly attenuates bone mass loss in mice. Our investigation underscores the pivotal significance and therapeutic potential of modulating the p53-miR17 family-Rankl axis in the treatment of inflammaging-associated osteoporosis.

Indexed as

Bone and BonesLiverMicroRNAsRANK LigandTumor Suppressor Protein p53AnimalsFemaleGene Expression RegulationHepatocytesHumansMaleMiceOsteoporosisSignal TransductionMicroRNAsMIRN17 microRNA, humanMirn17 microRNA, mouseRANK LigandTnfsf11 protein, mouseTumor Suppressor Protein p53inflammagingliver-bone communicationmiR17 familyosteoporosisp53Rankl

Identifiers

PMID40308192
PMCPMC11853355

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Registered trials

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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.