Evidence map›Paper›PMID 38486093›Full record

ArticleCommunications biology2024

Glutamine suppresses senescence and promotes autophagy through glycolysis inhibition-mediated AMPKα lactylation in intervertebral disc degeneration.

Yangyang Zhang, Zhengqi Huang, Weitao Han, Jiajun Wu, Shuangxing Li, Tianyu Qin, Chao Zhang, Ming Shi, Shun Han, Bo Gao and 4 more

Open access · goldAbstract read
In one paragraph

Article in Communications biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
20.0field-weighted citation impact, top 1% 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

60 citing papers in PubMed, 47 citations in OpenAlex.

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  19. [Glutamine-induced autophagy exacerbates muscle atrophy in cachectic nude mice: a multi-omics analysis].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026
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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

14 authors at 2 institutions in 2 countries.

Yangyang Zhang *Department of Spine Surgery, the First Affiliated Hospital of University of South China, Hengyang, 421200, China.
Zhengqi Huang *Department of Spine Surgery, Sun Yat-sen Memorial Hospital of Sun Yat-sen University, Guangzhou, 510289, China.
Weitao Han *Department of Spine Surgery, Sun Yat-sen Memorial Hospital of Sun Yat-sen University, Guangzhou, 510289, China.
Jiajun WuDepartment of Spine Surgery, Sun Yat-sen Memorial Hospital of Sun Yat-sen University, Guangzhou, 510289, China.
Shuangxing LiDepartment of Spine Surgery, Sun Yat-sen Memorial Hospital of Sun Yat-sen University, Guangzhou, 510289, China.
Tianyu QinDepartment of Spine Surgery, Sun Yat-sen Memorial Hospital of Sun Yat-sen University, Guangzhou, 510289, China.
Chao ZhangDepartment of Spine Surgery, Sun Yat-sen Memorial Hospital of Sun Yat-sen University, Guangzhou, 510289, China.
Ming ShiDepartment of Spine Surgery, Sun Yat-sen Memorial Hospital of Sun Yat-sen University, Guangzhou, 510289, China.
Shun HanDepartment of Spine Surgery, Sun Yat-sen Memorial Hospital of Sun Yat-sen University, Guangzhou, 510289, China.
Bo GaoDepartment of Spine Surgery, Sun Yat-sen Memorial Hospital of Sun Yat-sen University, Guangzhou, 510289, China.
Song JinDepartment of Orthopedics, the Eighth Affiliated Hospital of Sun Yat-sen University, Shenzhen, 518031, China.
Yin XiaoSchool of Medicine and Dentistry, Menzies Health Institute Queensland, Griffith University, Brisbane, QLD, Australia.
Kang XuGuangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Medical Research Center, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, 510289, China. xukang@mail.sysu.edu.cn.ORCID 0000-0002-5925-0130
Wei YeDepartment of Spine Surgery, Sun Yat-sen Memorial Hospital of Sun Yat-sen University, Guangzhou, 510289, China. yewei3@mail.sysu.edu.cn.ORCID 0000-0002-2908-1305
Sun Yat-sen University · CNGriffith University · AU

Funding

National Natural Science Foundation of China (National Science Foundation of China) 81572197National Natural Science Foundation of China (National Science Foundation of China) 82372437
6 · The paper itself

Abstract

Regulating metabolic disorders has become a promising focus in treating intervertebral disc degeneration (IDD). A few drugs regulating metabolism, such as atorvastatin, metformin, and melatonin, show positive effects in treating IDD. Glutamine participates in multiple metabolic processes, including glutaminolysis and glycolysis; however, its impact on IDD is unclear. The current study reveals that glutamine levels are decreased in severely degenerated human nucleus pulposus (NP) tissues and aging Sprague-Dawley (SD) rat nucleus pulposus tissues, while lactate accumulation and lactylation are increased. Supplementary glutamine suppresses glycolysis and reduces lactate production, which downregulates adenosine-5'-monophosphate-activated protein kinase α (AMPKα) lactylation and upregulates AMPKα phosphorylation. Moreover, glutamine treatment reduces NP cell senescence and enhances autophagy and matrix synthesis via inhibition of glycolysis and AMPK lactylation, and glycolysis inhibition suppresses lactylation. Our results indicate that glutamine could prevent IDD by glycolysis inhibition-decreased AMPKα lactylation, which promotes autophagy and suppresses NP cell senescence.

Indexed as

Intervertebral Disc DegenerationAMP-Activated Protein KinasesAnimalsAutophagyGlutamineHumansLactatesRatsRats, Sprague-DawleyAMP-Activated Protein KinasesGlutamineLactates

Identifiers

PMID38486093
PMCPMC10940657
OpenAlexW4392817955

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.