Evidence map›Paper›PMID 35088483›Full record

ArticleCell proliferation2022

Dysfunction of metabolic activity of bone marrow mesenchymal stem cells in aged mice.

Xiaoyu Li, Xue Wang, Chunmei Zhang, Jinsong Wang, Songlin Wang, Lei Hu

Open access · goldAbstract read
In one paragraph

Article in Cell proliferation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
6.3field-weighted citation impact, top 2% 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

41 citing papers in PubMed, 75 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

6 authors at 1 institution in 2 countries.

Xiaoyu LiMolecular Laboratory for Gene Therapy and Tooth Regeneration, Beijing Key Laboratory of Tooth Regeneration and Function Reconstruction, Capital Medical University School of Stomatology, Beijing, China.ORCID https://orcid.org/0000-0002-8177-1813
Xue WangMolecular Laboratory for Gene Therapy and Tooth Regeneration, Beijing Key Laboratory of Tooth Regeneration and Function Reconstruction, Capital Medical University School of Stomatology, Beijing, China.
Chunmei ZhangMolecular Laboratory for Gene Therapy and Tooth Regeneration, Beijing Key Laboratory of Tooth Regeneration and Function Reconstruction, Capital Medical University School of Stomatology, Beijing, China.
Jinsong WangMolecular Laboratory for Gene Therapy and Tooth Regeneration, Beijing Key Laboratory of Tooth Regeneration and Function Reconstruction, Capital Medical University School of Stomatology, Beijing, China.
Songlin WangMolecular Laboratory for Gene Therapy and Tooth Regeneration, Beijing Key Laboratory of Tooth Regeneration and Function Reconstruction, Capital Medical University School of Stomatology, Beijing, China.
Lei HuMolecular Laboratory for Gene Therapy and Tooth Regeneration, Beijing Key Laboratory of Tooth Regeneration and Function Reconstruction, Capital Medical University School of Stomatology, Beijing, China.ORCID https://orcid.org/0000-0002-4710-3707
Capital Medical University · CN

Funding

Beijing Advanced Innovation Center for Big Data-based Precision Medicine PXM2021_014226_000026Beijing Hospitals Authority of Hospitals' Mission Plan SML20151401Beijing Municipal Administration of Hospitals' Youth Program QML20191504Beijing Municipal Education Commission 119207020201Beijing Municipal Science & Technology Commission Z181100001718208Beijing Talents Fund 2018000021469G285National Natural Science Foundation of China 82001067National Natural Science Foundation of China 823030031National Natural Science Foundation of China 91649124Scientific Research Common Program of Beijing Municipal Commission of Education KM202110025009
6 · The paper itself

Abstract

objectivesEvidences have suggested that the metabolic function is the key regulator to the fate of MSCs, but its function in senescence of MSC and the underlying mechanism is unclear. Therefore, the purpose of this study was to investigate the metabolic activity of MSCs and its possible mechanism during aging. MATERIALS AND

methodsWe used the Seahorse XF24 Analyzer to understand OCR and ECAR in BMSCs and used RT-PCR to analyze the gene expression of mitochondrial biogenesis and key enzymes in glycolysis. We analyzed BMSC mitochondrial activity by MitoTracker Deep Red and JC-1 staining, and detected NAD+/NADH ratio and ATP levels in BMSCs. Microarray and proteomic analyses were performed to detect differentially expressed genes and proteins in BMSCs. The impact of aging on BMSCs through mitochondrial electron transport chain (ETC) was evaluated by Rotenone and Coenzyme Q10.

resultsOur results demonstrated that the oxidative phosphorylation and glycolytic activity of BMSCs in aged mice were significantly decreased when compared with young mice. BMSCs in aged mice had lower mitochondrial membrane potential, NAD+/NADH ratio, and ATP production than young mice. FABP4 may play a key role in BMSC senescence caused by fatty acid metabolism disorders.

conclusionsTaken together, our results indicated the dysfunction of the metabolic activity of BMSCs in aged mice, which would play the important role in the impaired biological properties. Therefore, the regulation of metabolic activity may be a potential therapeutic target for enhancing the regenerative functions of BMSCs.

Indexed as

AgingAnimalsBone Marrow CellsCell DifferentiationCells, CulturedMesenchymal Stem CellsMiceMitochondriaOsteogenesisagingbone marrow mesenchymal stem cellmetabolic activitymetabolismmitochondrialosteogenesis

Identifiers

PMID35088483
PMCPMC8891618
OpenAlexW4210490357

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.