Evidence map›Paper›PMID 42186485›Full record

ArticleJournal of tissue engineering

Chondrocyte metabolic transition from proliferation to quiescence revealed by FLIM in postnatal mouse knee joints.

Nadezda Ignatyeva, Boris Yakimov, Anastasiia D Kurenkova, Irina A Romanova, Pavel D Kibirskiy, Nikita Gavrilov, Anastasiya Patsyurkevich, Irina D Shcherbakova, Artem M Mozherov, Aleksandra V Kashina and 3 more

Abstract read
In one paragraph

Article in Journal of tissue engineering. 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

13 authors.

Nadezda IgnatyevaInstitute for Regenerative Medicine, Sechenov First Moscow State Medical University (Sechenov University), Russia.ORCID https://orcid.org/0009-0008-4421-0495
Boris YakimovInstitute for Regenerative Medicine, Sechenov First Moscow State Medical University (Sechenov University), Russia.
Anastasiia D KurenkovaInstitute for Regenerative Medicine, Sechenov First Moscow State Medical University (Sechenov University), Russia.
Irina A RomanovaInstitute for Regenerative Medicine, Sechenov First Moscow State Medical University (Sechenov University), Russia.
Pavel D KibirskiyInstitute for Regenerative Medicine, Sechenov First Moscow State Medical University (Sechenov University), Russia.
Nikita GavrilovInstitute for Regenerative Medicine, Sechenov First Moscow State Medical University (Sechenov University), Russia.
Anastasiya PatsyurkevichInstitute for Regenerative Medicine, Sechenov First Moscow State Medical University (Sechenov University), Russia.
Irina D ShcherbakovaInstitute for Regenerative Medicine, Sechenov First Moscow State Medical University (Sechenov University), Russia.
Artem M MozherovFederal State Budgetary Educational Institution of Higher Education "Privolzhsky Research Medical University", Ministry of Health of the Russian Federation, Nizhny Novgorod, Russia.
Aleksandra V KashinaFederal State Budgetary Educational Institution of Higher Education "Privolzhsky Research Medical University", Ministry of Health of the Russian Federation, Nizhny Novgorod, Russia.
Evgeny A ShirshinInstitute for Regenerative Medicine, Sechenov First Moscow State Medical University (Sechenov University), Russia.
Peter S TimashevInstitute for Regenerative Medicine, Sechenov First Moscow State Medical University (Sechenov University), Russia.
Ekaterina V MedvedevaInstitute for Regenerative Medicine, Sechenov First Moscow State Medical University (Sechenov University), Russia.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Adult articular cartilage chondrocytes have a limited capacity to divide compared to juvenile cells, but the mechanisms behind this decline remain unclear. This study investigates metabolic changes associated with the cessation of chondrocyte proliferation in mouse articular cartilage. Using 5-ethynyl-2'-deoxyuridine (EdU) labeling, the postnatal decline in proliferation was tracked. Label-free fluorescence-lifetime imaging microscopy (FLIM) method, combined with artificial intelligence (AI)-assisted image segmentation, was applied to live cartilage sections to analyze metabolic parameters. Results showed that 1-month-old articular cartilage chondrocytes enter quiescence with significant changes in FLIM fluorescence decay parameters across cartilage zones compared to juvenile chondrocytes. Chondroprogenitors in the superficial zone showed a gradual decrease in citrate synthase content, while glycolytic activity increased with tissue depth. These findings reveal metabolic reprogramming that enables chondrocytes to adapt their metabolism despite limited oxygen availability to meet functional demands. Investigating these chondrocyte adaptations provides key insights for identifying metabolic targets and improving the design of durable, well-integrated tissue-engineered cartilage.

Indexed as

articular cartilage chondrocytesaxitinibchondroprogenitor proliferationenergy metabolismFLIM

Identifiers

PMID42186485
PMCPMC13198642

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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.