Evidence map›Paper›PMID 41694579›Full record

ArticleInternational journal of biological sciences2026

AMPKα1 Deficiency in Macrophages Impairs Tendon Regeneration and Tendon Stem Cell Function via TNF-α-FBP2 Signaling.

Lisha Zhu, Yu Wang, Xinmeng Shi, Min Yu, Xinjia Cai, Liyuan Chen, He Zhang, Xiaolan Wu, Chengye Ding, Hangbo Liu and 5 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of biological sciences, 2026. 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.

No citing paper in PubMed yet.

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

15 authors.

Lisha ZhuCentral Laboratory, Peking University School and Hospital of Stomatology, Beijing 100081, China.
Yu WangDepartment of Orthodontics, Peking University School and Hospital of Stomatology, Beijing 100081, China.
Xinmeng ShiDepartment of Orthodontics, Peking University School and Hospital of Stomatology, Beijing 100081, China.
Min YuCentral Laboratory, Peking University School and Hospital of Stomatology, Beijing 100081, China.
Xinjia CaiCentral Laboratory, Peking University School and Hospital of Stomatology, Beijing 100081, China.
Liyuan ChenDepartment of Orthodontics, Peking University School and Hospital of Stomatology, Beijing 100081, China.
He ZhangDepartment of Orthodontics, Peking University School and Hospital of Stomatology, Beijing 100081, China.
Xiaolan WuDepartment of Orthodontics, Peking University School and Hospital of Stomatology, Beijing 100081, China.
Chengye DingDepartment of Orthodontics, Peking University School and Hospital of Stomatology, Beijing 100081, China.
Hangbo LiuDepartment of Orthodontics, Peking University School and Hospital of Stomatology, Beijing 100081, China.
Shiying ZhangDepartment of Orthodontics, Peking University School and Hospital of Stomatology, Beijing 100081, China.
Chang LiDepartment of Orthodontics, Peking University School and Hospital of Stomatology, Beijing 100081, China.
Tianhao WuDepartment of Orthodontics, Peking University School and Hospital of Stomatology, Beijing 100081, China.
Nan JiangCentral Laboratory, Peking University School and Hospital of Stomatology, Beijing 100081, China.
Yan LiuCentral Laboratory, Peking University School and Hospital of Stomatology, Beijing 100081, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tendon healing is limited by the minimal intrinsic regenerative capacity of the tissue, resulting in the formation of fibrovascular scar tissue rather than functional regeneration. Macrophage immunometabolism governs the balance between inflammation and repair; however, its effects on tendon regeneration are poorly understood. In this study, we investigated the differential activation of macrophage AMP-activated protein kinase (AMPK) and its phenotypic alterations in neonatal and adult tendon injury models. Using myeloid-specific AMPKα1 knockout (

Indexed as

AMP-Activated Protein KinasesMacrophagesRegenerationStem CellsTendonsTumor Necrosis Factor-alphaAnimalsCell ProliferationMiceMice, KnockoutSignal TransductionTendon InjuriesAMP-Activated Protein KinasesPrkaa1 protein, mouseTumor Necrosis Factor-alphaadenosine monophosphate-activated protein kinasefructose-1,6-bisphosphatase 2macrophagetendon regenerationtendon stem/progenitor cells

Identifiers

PMID41694579
PMCPMC12905647

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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.