Evidence map›Paper›PMID 38840443›Full record

ArticleAging cell2024

Pip5k1γ promotes anabolism of nucleus pulposus cells and intervertebral disc homeostasis by activating CaMKII-Ampk pathway in aged mice.

Mingjue Chen, Feiyun Li, Minghao Qu, Xiaowan Jin, Tailin He, Shuangshuang He, Sheng Chen, Qing Yao, Lin Wang, Di Chen and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Aging cell, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

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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

12 authors.

Mingjue ChenDepartment of Biochemistry, School of Medicine, Shenzhen Key Laboratory of Cell Microenvironment, Guangdong Provincial Key Laboratory of Cell Microenvironment and Disease Research, Southern University of Science and Technology, Shenzhen, China.ORCID 0000-0002-9340-4092
Feiyun LiDepartment of Biochemistry, School of Medicine, Shenzhen Key Laboratory of Cell Microenvironment, Guangdong Provincial Key Laboratory of Cell Microenvironment and Disease Research, Southern University of Science and Technology, Shenzhen, China.
Minghao QuSchool of Medicine, Southern University of Science and Technology, Shenzhen, China.
Xiaowan JinDepartment of Biochemistry, School of Medicine, Shenzhen Key Laboratory of Cell Microenvironment, Guangdong Provincial Key Laboratory of Cell Microenvironment and Disease Research, Southern University of Science and Technology, Shenzhen, China.
Tailin HeDepartment of Biochemistry, School of Medicine, Shenzhen Key Laboratory of Cell Microenvironment, Guangdong Provincial Key Laboratory of Cell Microenvironment and Disease Research, Southern University of Science and Technology, Shenzhen, China.
Shuangshuang HeDepartment of Biochemistry, School of Medicine, Shenzhen Key Laboratory of Cell Microenvironment, Guangdong Provincial Key Laboratory of Cell Microenvironment and Disease Research, Southern University of Science and Technology, Shenzhen, China.
Sheng ChenDepartment of Orthopaedics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Qing YaoDepartment of Biochemistry, School of Medicine, Shenzhen Key Laboratory of Cell Microenvironment, Guangdong Provincial Key Laboratory of Cell Microenvironment and Disease Research, Southern University of Science and Technology, Shenzhen, China.
Lin WangSchool of Medicine, Southern University of Science and Technology, Shenzhen, China.
Di ChenResearch Center for Human Tissues and Organs Degeneration, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen, China.
Xiaohao WuDivision of Immunology and Rheumatology, Stanford University, Stanford, California, USA.
Guozhi XiaoDepartment of Biochemistry, School of Medicine, Shenzhen Key Laboratory of Cell Microenvironment, Guangdong Provincial Key Laboratory of Cell Microenvironment and Disease Research, Southern University of Science and Technology, Shenzhen, China.

Funding

Guangdong Provincial Department of Science and Technology 2017B030301018Medical Research Innovation Project G030410001National Key Research and Development Program of China 2019YFA0906004National Natural Science Foundation of China 81991513National Natural Science Foundation of China 82230081National Natural Science Foundation of China 82250710175National Natural Science Foundation of China 8226116039National Natural Science Foundation of China 82302767Shenzhen Fundamental Research Program JCYJ20220818100617036Wuhan Union Hospital 2022xhyn032
6 · The paper itself

Abstract

Degenerative disc disease (DDD) represents a significant global health challenge, yet its underlying molecular mechanisms remain elusive. This study aimed to investigate the role of type 1 phosphatidylinositol 4-phosphate 5-kinase (Pip5k1) in intervertebral disc (IVD) homeostasis and disease. All three Pip5k1 isoforms, namely Pip5k1α, Pip5k1β, and Pip5k1γ, were detectable in mouse and human IVD tissues, with Pip5k1γ displaying a highest expression in nucleus pulposus (NP) cells. The expression of Pip5k1γ was significantly down-regulated in the NP cells of aged mice and patients with severe DDD. To determine whether Pip5k1γ expression is required for disc homeostasis, we generated a Pip5k1γ

Indexed as

HomeostasisIntervertebral DiscNucleus PulposusPhosphotransferases (Alcohol Group Acceptor)AgingAMP-Activated Protein KinasesAnimalsHumansIntervertebral Disc DegenerationMiceSignal Transduction1-phosphatidylinositol-4-phosphate 5-kinaseAMP-Activated Protein KinasesPhosphotransferases (Alcohol Group Acceptor)agingAmpkCaMKIIdisc degenerationmetforminnucleus pulposusPip5k1γ

Identifiers

PMID38840443
PMCPMC11488325

What Socratic 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 Socratic graph.