Evidence map›Paper›PMID 41046114›Full record

ArticleBone2026

FGF8 induces bone and joint regeneration at digit amputation wounds in neonate mice.

Ling Yu, Mingquan Yan, Sarah M Wolff, Joseph D Knue, Hannah M Smith, Connor P Dolan, Ken Muneoka, Selim Romero, James J Cai, Carissa Yun and 3 more

Abstract read
In one paragraph

Article in Bone, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Enhancer-directed gene delivery for digit regeneration based on conserved epidermal factors.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  2. Article
  3. 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

13 authors.

Ling YuDepartment of Veterinary Physiology and Pharmacology, College of Veterinary Medicine and Biomedical Sciences, Texas A&M University, College Station, TX, 77843, USA. Electronic address: lyu@cvm.tamu.edu.
Mingquan YanDepartment of Veterinary Physiology and Pharmacology, College of Veterinary Medicine and Biomedical Sciences, Texas A&M University, College Station, TX, 77843, USA. Electronic address: myan@cvm.tamu.edu.
Sarah M WolffDepartment of Veterinary Physiology and Pharmacology, College of Veterinary Medicine and Biomedical Sciences, Texas A&M University, College Station, TX, 77843, USA. Electronic address: swolff@tamu.edu.
Joseph D KnueDepartment of Veterinary Physiology and Pharmacology, College of Veterinary Medicine and Biomedical Sciences, Texas A&M University, College Station, TX, 77843, USA. Electronic address: jdknue@cvm.tamu.edu.
Hannah M SmithDepartment of Veterinary Physiology and Pharmacology, College of Veterinary Medicine and Biomedical Sciences, Texas A&M University, College Station, TX, 77843, USA. Electronic address: hsmith314@exchange.tamu.edu.
Connor P DolanDepartment of Veterinary Physiology and Pharmacology, College of Veterinary Medicine and Biomedical Sciences, Texas A&M University, College Station, TX, 77843, USA. Electronic address: connor.dolan@asu.edu.
Ken MuneokaDepartment of Veterinary Physiology and Pharmacology, College of Veterinary Medicine and Biomedical Sciences, Texas A&M University, College Station, TX, 77843, USA. Electronic address: kmuneoka@cvm.tamu.edu.
Selim RomeroDepartment of Veterinary Integrative Biosciences, College of Veterinary Medicine and Biomedical Sciences, Texas A&M University, College Station, TX, 77843, USA. Electronic address: ssromerogon@tamu.edu.
James J CaiDepartment of Veterinary Integrative Biosciences, College of Veterinary Medicine and Biomedical Sciences, Texas A&M University, College Station, TX, 77843, USA. Electronic address: jcai@tamu.edu.
Carissa YunTexas A&M Institute for Genome Sciences & Society, College Station, TX, 77843, USA. Electronic address: carissa.yun@exchange.tamu.edu.
Devon J BolandTexas A&M Institute for Genome Sciences & Society, College Station, TX, 77843, USA. Electronic address: devonjboland@tamu.edu.
Regina BrunauerDepartment of Veterinary Physiology and Pharmacology, College of Veterinary Medicine and Biomedical Sciences, Texas A&M University, College Station, TX, 77843, USA; LBG Ludwig Boltzmann Institute for Traumatology, The Research Center in Cooperation with AUVA, 1200, Vienna, Austria; Austrian Cluster for Tissue Regeneration, 1200, Vienna, Austria. Electronic address: regina.brunauer@trauma.lbg.ac.at.
Lindsay A DawsonDepartment of Veterinary Physiology and Pharmacology, College of Veterinary Medicine and Biomedical Sciences, Texas A&M University, College Station, TX, 77843, USA. Electronic address: Ldawson@cvm.tamu.edu.

Funding

Determining cell-specific mechanisms that drive aberrant bone regeneration in Down syndromeRF1AG081812 · NIA · TEXAS A&M AGRILIFE RESEARCH · PI DAWSON, LINDSAY A · 2023 to 2023
$1.6M
IMSD at Texas A&M University: Initiative for Maximizing Student Diversity in Biomedical SciencesT32GM135748 · NIGMS · TEXAS A&M UNIVERSITY · PI BRINKMEYER-LANGFORD, CANDICE L., CHIU, WEIHSUEH A · 2020 to 2024
$1.2M
Veterinary Student Research TrainingT35OD010991 · OD · TEXAS A&M AGRILIFE RESEARCH · PI GADDY, DANA · 2012 to 2025
$920k
Determining cell-specific mechanisms that drive aberrant bone regeneration in Down syndromeR01AG081812 · NIA · TEXAS A&M AGRILIFE RESEARCH · PI Lindsay A Dawson · 2026 to 2026
$496k
NIA NIH HHS R01 AG081812NIA NIH HHS RF1 AG081812NIGMS NIH HHS T32 GM135748NIH HHS T35 OD010991
6 · The paper itself

Abstract

Due to increases in vascular diseases, the incidence of limb loss is predicted to more than double in the next quarter century. Therefore, developing a greater understanding of the latent regenerative capacity in mammals is a significant and growing goal. Mammals, including humans and mice, have limited regenerative capacity following limb amputation, with regenerative responses restricted to amputations transecting the distal digit tip (P3). Unlike P3, amputations of the adjacent skeletal segment, the middle phalanx, P2, are non-regenerative and result in bone truncation and soft tissue scar formation. As such, P2 amputation is a simple yet powerful model to test strategies for inducing mammalian musculoskeletal regeneration from an otherwise non-regenerative amputation plane. Here, we report that Fibroblast Growth Factor 8 (FGF8) drives synovial joint regeneration at P2 amputation wounds in neonate mice. This response is characterized by the regeneration of a synovial cavity, a skeletal nodule lined with articular cartilage, and tendon and ligament regeneration. FGF8 also induces cartilage formation on the P2 stump that serves as a template for partial P2 bone regeneration, thus FGF8 drives the composite regeneration of stump and joint tissues. FGF8-induced joint regeneration is associated with the upregulation of several, but not all, genes that characterize joint development, and is morphologically distinct from digit joint development. Lineage tracing studies demonstrate that cells at the amputation wound contribute to the regenerated joint structures. These studies provide evidence that the otherwise non-regenerative P2 amputation wound possesses tremendous regenerative capacity that is dormant under normal circumstances.

Indexed as

Amputation, SurgicalBone RegenerationFibroblast Growth Factor 8JointsRegenerationAnimalsAnimals, NewbornMiceMice, Inbred C57BLWound HealingFibroblast Growth Factor 8BoneCartilageEndochondral ossificationFGF8Joint morphogenesisJoint regeneration

Identifiers

PMID41046114
PMCPMC13029017

What OpenQuestion holds

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LicenceCC BY
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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.