Evidence map›Paper›PMID 35461310›Full record

ArticleCell death & disease2022

Autophagy guards tendon homeostasis.

Costanza Montagna, Rene B Svensson, Monika L Bayer, Salvatore Rizza, Emiliano Maiani, Ching-Yan Chloé Yeung, Giuseppe Filomeni, Michael Kjær

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2022. 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
2.9field-weighted citation impact, top 9% 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, 18 citations in OpenAlex.

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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 at 4 institutions in 2 countries.

Costanza MontagnaInstitute of Sports Medicine Copenhagen, Department of Orthopedic Surgery, Copenhagen University Hospital-Bispebjerg and Frederiksberg, Copenhagen, Denmark. costanza.montagna@unicamillus.org.ORCID 0000-0001-9309-1666
Rene B SvenssonInstitute of Sports Medicine Copenhagen, Department of Orthopedic Surgery, Copenhagen University Hospital-Bispebjerg and Frederiksberg, Copenhagen, Denmark.
Monika L BayerInstitute of Sports Medicine Copenhagen, Department of Orthopedic Surgery, Copenhagen University Hospital-Bispebjerg and Frederiksberg, Copenhagen, Denmark.
Salvatore RizzaRedox Signaling and Oxidative Stress Group, Danish Cancer Society Research Center, Copenhagen, Denmark.ORCID 0000-0001-7335-4684
Emiliano MaianiUnicamillus-Saint Camillus, University of Health Sciences, Rome, Italy.
Ching-Yan Chloé YeungInstitute of Sports Medicine Copenhagen, Department of Orthopedic Surgery, Copenhagen University Hospital-Bispebjerg and Frederiksberg, Copenhagen, Denmark.
Giuseppe FilomeniCenter for Healthy Aging, Department of Clinical Medicine, University of Copenhagen, Copenhagen, Denmark.ORCID 0000-0002-2719-1412
Michael KjærInstitute of Sports Medicine Copenhagen, Department of Orthopedic Surgery, Copenhagen University Hospital-Bispebjerg and Frederiksberg, Copenhagen, Denmark.
University of Copenhagen · DKUniversity of Rome Tor Vergata · ITDanish Cancer Society · DKSaint Camillus International University of Health and Medical Sciences · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tendons are vital collagen-dense specialized connective tissues transducing the force from skeletal muscle to the bone, thus enabling movement of the human body. Tendon cells adjust matrix turnover in response to physiological tissue loading and pathological overloading (tendinopathy). Nevertheless, the regulation of tendon matrix quality control is still poorly understood and the pathogenesis of tendinopathy is presently unsolved. Autophagy, the major mechanism of degradation and recycling of cellular components, plays a fundamental role in the homeostasis of several tissues. Here, we investigate the contribution of autophagy to human tendons' physiology, and we provide in vivo evidence that it is an active process in human tendon tissue. We show that selective autophagy of the endoplasmic reticulum (ER-phagy), regulates the secretion of type I procollagen (PC1), the major component of tendon extracellular matrix. Pharmacological activation of autophagy by inhibition of mTOR pathway alters the ultrastructural morphology of three-dimensional tissue-engineered tendons, shifting collagen fibrils size distribution. Moreover, autophagy induction negatively affects the biomechanical properties of the tissue-engineered tendons, causing a reduction in mechanical strength under tensile force. Overall, our results provide the first evidence that autophagy regulates tendon homeostasis by controlling PC1 quality control, thus potentially playing a role in the development of injured tendons.

Indexed as

AutophagyTendinopathyTendonsCollagenHomeostasisHumansCollagen

Identifiers

PMID35461310
PMCPMC9035152
OpenAlexW4224253054

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.