Evidence map›Paper›PMID 42169959›Full record

ArticleJournal of orthopaedic translation2026

Talin1 loss activates DRG neurons to accelerate bone remodeling and fracture healing in mice.

Qinnan Yan, Donghao Gan, Kangtai Xu, Zecai Chen, Sixiong Lin, Bo Zhou, Zhen Xu, Qiyue Zhong, Chu Tao, Yiming Zhong and 6 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of orthopaedic translation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. Article
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

16 authors.

Qinnan YanDepartment of Biochemistry, Homeostatic Medicine Institute, School of Medicine, Guangdong Provincial Key Laboratory of Cell Microenvironment and Disease Research, Shenzhen Key Laboratory of Cell Microenvironment, Southern University of Science and Technology, Shenzhen, 518055, China.
Donghao GanDepartment of Biochemistry, Homeostatic Medicine Institute, School of Medicine, Guangdong Provincial Key Laboratory of Cell Microenvironment and Disease Research, Shenzhen Key Laboratory of Cell Microenvironment, Southern University of Science and Technology, Shenzhen, 518055, China.
Kangtai XuDepartment of Medical Neuroscience, School of Medicine, Southern University of Science and Technology, Shenzhen, 518055, China.
Zecai ChenDepartment of Orthopaedics, Shenzhen Nanshan People's Hospital, Affiliated Nanshan Hospital of Shenzhen University, Shenzhen, Guangdong Province, China.
Sixiong LinDepartment of Biochemistry, Homeostatic Medicine Institute, School of Medicine, Guangdong Provincial Key Laboratory of Cell Microenvironment and Disease Research, Shenzhen Key Laboratory of Cell Microenvironment, Southern University of Science and Technology, Shenzhen, 518055, China.
Bo ZhouLaboratory of Oral Homeostatic Medicine, Homeostatic Medicine Institute, School of Medicine, Southern University of Science and Technology, Shenzhen, 518055, China.
Zhen XuDepartment of Orthopaedics, Shenzhen Nanshan People's Hospital, Affiliated Nanshan Hospital of Shenzhen University, Shenzhen, Guangdong Province, China.
Qiyue ZhongDepartment of Biochemistry, Homeostatic Medicine Institute, School of Medicine, Guangdong Provincial Key Laboratory of Cell Microenvironment and Disease Research, Shenzhen Key Laboratory of Cell Microenvironment, Southern University of Science and Technology, Shenzhen, 518055, China.
Chu TaoDepartment of Biochemistry, Homeostatic Medicine Institute, School of Medicine, Guangdong Provincial Key Laboratory of Cell Microenvironment and Disease Research, Shenzhen Key Laboratory of Cell Microenvironment, Southern University of Science and Technology, Shenzhen, 518055, China.
Yiming ZhongDepartment of Biochemistry, Homeostatic Medicine Institute, School of Medicine, Guangdong Provincial Key Laboratory of Cell Microenvironment and Disease Research, Shenzhen Key Laboratory of Cell Microenvironment, Southern University of Science and Technology, Shenzhen, 518055, China.
Shaochuan HuoResearch Institute, Shenzhen Hospital (Futian) of Guangzhou University of Chinese Medicine, Shenzhen, China.
Weihong YiDepartment of Orthopaedics, Shenzhen Nanshan People's Hospital, Affiliated Nanshan Hospital of Shenzhen University, Shenzhen, Guangdong Province, China.
Zilong WangDepartment of Medical Neuroscience, School of Medicine, Southern University of Science and Technology, Shenzhen, 518055, China.
Xuejun SongDepartment of Medical Neuroscience, School of Medicine, Southern University of Science and Technology, Shenzhen, 518055, China.
Lei QinDepartment of Orthopaedics, Shenzhen Nanshan People's Hospital, Affiliated Nanshan Hospital of Shenzhen University, Shenzhen, Guangdong Province, China.
Guozhi XiaoDepartment of Biochemistry, Homeostatic Medicine Institute, School of Medicine, Guangdong Provincial Key Laboratory of Cell Microenvironment and Disease Research, Shenzhen Key Laboratory of Cell Microenvironment, Southern University of Science and Technology, Shenzhen, 518055, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Bone tissue is densely innervated by sensory nerve fibers, whose roles in bone remodeling and regeneration are poorly defined. This study aims to investigate the physiological function of Talin1, a key focal adhesion protein, in dorsal root ganglion (DRG) neurons in pain processing and its specific impact on bone remodeling and fracture healing. Materials and methods: We utilized a transgenic mouse model ( Results: Talin1 is predominantly expressed in C-fiber DRG neurons and its expression is significantly downregulated following bone fracture. Talin1 loss markedly activates DRG sensory neurons and increases mechanical, but not thermal, pain sensitivity in mice. Concurrently, Talin1 deficiency inhibits mitophagy and impairs mitochondrial function, as indicated by altered mitochondrial morphology, abnormal reactive oxygen species production and reduced mitochondrial membrane potential. Furthermore, beyond its role in nociception, Talin1 loss not only increases bone mass in both adult and aged mice but also accelerates fracture healing by modulating bone remodeling. This pro-healing phenotype coincides with increased expression of calcitonin gene-related peptide (CGRP) in DRG neurons. Critically, pharmacological inhibition of CGRP receptors at the fracture site by BIBN abolishes the fracture healing-promoting effect caused by Talin1 loss. Conclusions: Our studies demonstrate that Talin1 plays a pivotal role in modulating sensory neuron activation, pain perception, and bone remodeling. Specifically, Talin1 loss accelerates bone repair by upregulating CGRP, thereby establishing a Talin1-CGRP signaling axis that mediates sensory neuron control of fracture healing. The translational potential of this article: This research highlights the dual role of Talin1 in sensory neurons in modulating both pain perception and bone remodeling, and emphasizes the potential for targeting Talin1 signaling as a therapeutic strategy to alleviate pain or to accelerate fracture healing.

Indexed as

Bone remodelingDorsal root ganglion (DRG) neuronFracture healingMitophagyPain perceptionTalin1

Identifiers

PMID42169959
PMCPMC13187541

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.