Evidence map›Paper›PMID 31574189›Full record

ArticleStem cells (Dayton, Ohio)2019

Mitochondrial Phosphoenolpyruvate Carboxykinase Regulates Osteogenic Differentiation by Modulating AMPK/ULK1-Dependent Autophagy.

Zheng Li, Xuenan Liu, Yuan Zhu, Yangge Du, Xuejiao Liu, Longwei Lv, Xiao Zhang, Yunsong Liu, Ping Zhang, Yongsheng Zhou

Open access · hybridAbstract read
In one paragraph

Article in Stem cells (Dayton, Ohio), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

16 citing papers in PubMed, 22 citations in OpenAlex.

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  11. Frontiers in plant science · 2022
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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

10 authors at 1 institution in 1 country.

Zheng LiDepartment of Prosthodontics, School and Hospital of Stomatology, Peking University, Beijing, People's Republic of China.ORCID 0000-0003-0215-4401
Xuenan LiuDepartment of Prosthodontics, School and Hospital of Stomatology, Peking University, Beijing, People's Republic of China.
Yuan ZhuDepartment of Prosthodontics, School and Hospital of Stomatology, Peking University, Beijing, People's Republic of China.
Yangge DuDepartment of Prosthodontics, School and Hospital of Stomatology, Peking University, Beijing, People's Republic of China.
Xuejiao LiuDepartment of Prosthodontics, School and Hospital of Stomatology, Peking University, Beijing, People's Republic of China.
Longwei LvDepartment of Prosthodontics, School and Hospital of Stomatology, Peking University, Beijing, People's Republic of China.
Xiao ZhangDepartment of Prosthodontics, School and Hospital of Stomatology, Peking University, Beijing, People's Republic of China.
Yunsong LiuDepartment of Prosthodontics, School and Hospital of Stomatology, Peking University, Beijing, People's Republic of China.
Ping ZhangDepartment of Prosthodontics, School and Hospital of Stomatology, Peking University, Beijing, People's Republic of China.
Yongsheng ZhouDepartment of Prosthodontics, School and Hospital of Stomatology, Peking University, Beijing, People's Republic of China.
Peking University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondrial phosphoenolpyruvate carboxykinase (PCK2) is a rate-limiting enzyme that plays critical roles in multiple physiological processes. The decompensation of PCK2 leads to various energy metabolic disorders. However, little is known regarding the effects of PCK2 on osteogenesis by human mesenchymal stem cells (hMSCs). Here, we report a novel function of PCK2 as a positive regulator of MSCs osteogenic differentiation. In addition to its well-known role in anabolism, we demonstrate that PCK2 regulates autophagy. PCK2 deficiency significantly suppressed autophagy, leading to the impairment of osteogenic capacity of MSCs. On the other hand, autophagy was promoted by PCK2 overexpression; this was accompanied by increased osteogenic differentiation of MSCs. Moreover, PCK2 regulated osteogenic differentiation of MSCs via AMP-activated protein kinase (AMPK)/unc-51 like autophagy activating kinase 1(ULK1)-dependent autophagy. Collectively, our present study unveiled a novel role for PCK2 in integrating autophagy and bone formation, providing a potential target for stem cell-based bone tissue engineering that may lead to improved therapies for metabolic bone diseases. Stem Cells 2019;37:1542-1555.

Indexed as

AMP-Activated Protein KinasesAutophagyAutophagy-Related Protein-1 HomologBone and BonesBone DevelopmentCell LineHumansIntracellular Signaling Peptides and ProteinsMesenchymal Stem CellsMitochondriaOsteogenesisPhosphoenolpyruvate Carboxykinase (GTP)RNA InterferenceRNA, Small InterferingAMP-Activated Protein KinasesAutophagy-Related Protein-1 HomologIntracellular Signaling Peptides and ProteinsPhosphoenolpyruvate Carboxykinase (GTP)RNA, Small InterferingULK1 protein, humanAutophagyMesenchymal stem cellsMitochondrial phosphoenolpyruvate carboxykinaseOsteogenic differentiation

Identifiers

PMID31574189
PMCPMC6916635
OpenAlexW2978012731

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.