Evidence map›Paper›PMID 34592976›Full record

ArticleBMC musculoskeletal disorders2021

TGF-β3 regulates adhesion formation through the JNK/c-Jun pathway during flexor tendon healing.

Ke Jiang, Yuling Li, Chao Xiang, Yan Xiong, Jiameng Jia

Open access · goldAbstract read
In one paragraph

Article in BMC musculoskeletal disorders, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.8field-weighted citation impact, top 10% of its field
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

15 citing papers in PubMed, 23 citations in OpenAlex.

  1. Predictors of postoperative complications in extensor tendon repairs.Turkish journal of physical medicine and rehabilitation · 2026
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  8. Peritendinous adhesion: Therapeutic targets and progress of drug therapy.Computational and structural biotechnology journal · 2024
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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

5 authors at 2 institutions in 1 country.

Ke JiangDepartment of Orthopaedics, Affilliated Hospital of North Sichuan Medical College, 63 Wenhua Road, Nanchong, Sichuan, 637000, People's Republic of China.
Yuling LiDepartment of Orthopaedics, Affilliated Hospital of North Sichuan Medical College, 63 Wenhua Road, Nanchong, Sichuan, 637000, People's Republic of China. lyl1987@nsmc.edu.cn.
Chao XiangDepartment of Orthopaedics, Affilliated Hospital of North Sichuan Medical College, 63 Wenhua Road, Nanchong, Sichuan, 637000, People's Republic of China.
Yan XiongDepartment of Orthopaedics, Daping Hospital, Army Medical University, Chongqing, 400042, People's Republic of China.
Jiameng JiaDepartment of Rehabilitation, Affilliated Hospital of North Sichuan Medical College, Nanchong, Sichuan, 637000, People's Republic of China.
North Sichuan Medical University · CNArmy Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe injured flexor tendon has poor healing ability, which is easy to cause tendon adhesion. It can affect the recovery of tendon function, which is still a long-term and difficult task for surgeons. Transforming growth factor β (TGF-β) has been widely considered to play an important role in flexor tendon repair in recent years.

aimThis work was to investigate the anti-adhesion and anti-inflammatory effects of TGF-β3 on flexor digitorum longus (FDL) tendon repair rats.

methodAnastomosis models of tendon laceration in the flexion toes of rats were delivered with no treatment, vehicle, or TGF-β3 -overexpressed adenovirus vector (ad-TGF-β3) locally to the injured tendon area from day 3 to 8. Subsequently, the expression of TGF-β3, TGF-β1/2, Smad3, Smad7, JNK, phosphorylation (p)-JNK, c-Jun, and phosphorylation (p)-c-Jun were detected by western blot, the expression of Mmp9 and Mmp2 by RT-qPCR, the Range of motion (ROM) and gliding resistance by adhesion formation testing, the mechanical strength of tendon healing by biomechanical testing, the pathologic changes of flexor tendon tissues by HE staining, the expression of collagen type III by immunohistochemical staining, and the levels of IL-6, TNF-α, COX2 and IL-1β in serum by ELISA, respectively.

resultsRat models treated with no treatment showed a lower elevation of TGF-β3 and Smad7 expression, and a higher elevation of TGF-β1/2 and Smad3 expression, during day 14 to day 28. Besides, under the treatment of ad-TGF-β3, a significantly increase was reflected in the expression of TGF-β3 and Smad7, ROM, as well as mechanical strength of flexor tendon, whereas significantly reduction was shown in gliding resistance, the content of inflammatory cytokines, the ratio of p-JNK/JNK, p-c-Jun/c-Jun, as well as the expression of TGF-β1/2, Smad3, Mmp9, and Mmp2 genes, as compared to those from vehicle treatment. Meanwhile, TGF-β3 demonstrated a better pathologic recovery process with no obvious necrosis or fracture of collagen fibers. Besides, TGF-β3 revealed a significant reduction of collagen type-III expression in the flexor tendon healing tissues.

conclusionThese findings suggested that TGF-β3 effectively protected against flexor tendon injury via regulating adhesion formation.

Indexed as

Tendon InjuriesTransforming Growth Factor beta3AnimalsRatsTendonsTissue AdhesionsTransforming Growth Factor beta1Wound HealingTransforming Growth Factor beta1Transforming Growth Factor beta3Adhesion formationFlexor tendonRepairTGF-β3

Identifiers

PMID34592976
PMCPMC8485513
OpenAlexW3111439519

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.