Evidence map›Paper›PMID 40820799›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025

Integrative Omics Reveals Glutamine Catabolism-Driven Apoptotic Suppression in Monocytes upon Mechanical Unloading.

Yi Ding, Fan Tong, Mingqiu Liu, Pin Yang, Jing Zeng, Yinghua Wei, Chunlin Li, Dong Li, Cheng Chang, Yangjun Zhang and 5 more

Abstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. Article
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

15 authors.

Yi DingState Key Laboratory of Medical Proteomics, Beijing Proteome Research Center, National Center for Protein Sciences (Beijing), Beijing Institute of Lifeomics, Beijing, 102206, China.
Fan TongState Key Laboratory of Medical Proteomics, Beijing Proteome Research Center, National Center for Protein Sciences (Beijing), Beijing Institute of Lifeomics, Beijing, 102206, China.
Mingqiu LiuState Key Laboratory of Medical Proteomics, Beijing Proteome Research Center, National Center for Protein Sciences (Beijing), Beijing Institute of Lifeomics, Beijing, 102206, China.
Pin YangSchool of Basic Medical Sciences, Anhui Medical University, Hefei, Anhui, 230022, China.
Jing ZengDepartment of Endocrinology, The Second Medical Center & National Clinical Research Center for Geriatric Diseases, Chinese PLA General Hospital, Beijing, 100036, China.
Yinghua WeiState Key Laboratory of Medical Proteomics, Beijing Proteome Research Center, National Center for Protein Sciences (Beijing), Beijing Institute of Lifeomics, Beijing, 102206, China.
Chunlin LiDepartment of Endocrinology, The Second Medical Center & National Clinical Research Center for Geriatric Diseases, Chinese PLA General Hospital, Beijing, 100036, China.
Dong LiState Key Laboratory of Medical Proteomics, Beijing Proteome Research Center, National Center for Protein Sciences (Beijing), Beijing Institute of Lifeomics, Beijing, 102206, China.
Cheng ChangState Key Laboratory of Medical Proteomics, Beijing Proteome Research Center, National Center for Protein Sciences (Beijing), Beijing Institute of Lifeomics, Beijing, 102206, China.
Yangjun ZhangState Key Laboratory of Medical Proteomics, Beijing Proteome Research Center, National Center for Protein Sciences (Beijing), Beijing Institute of Lifeomics, Beijing, 102206, China.
Shaoqiong YiState Key Laboratory of Medical Proteomics, Beijing Proteome Research Center, National Center for Protein Sciences (Beijing), Beijing Institute of Lifeomics, Beijing, 102206, China.
Fan HuDepartment of Endocrinology, The Second Medical Center & National Clinical Research Center for Geriatric Diseases, Chinese PLA General Hospital, Beijing, 100036, China.
Wenjie ShuBioinformatics Center of AMMS, Beijing, 100850, China.
Lingqiang ZhangState Key Laboratory of Medical Proteomics, Beijing Proteome Research Center, National Center for Protein Sciences (Beijing), Beijing Institute of Lifeomics, Beijing, 102206, China.
Chun-Ping CuiState Key Laboratory of Medical Proteomics, Beijing Proteome Research Center, National Center for Protein Sciences (Beijing), Beijing Institute of Lifeomics, Beijing, 102206, China.ORCID https://orcid.org/0000-0003-0251-3259

Funding

National Key R&D Program of China 2021YFA1300200National Key R&D Program of China 2022YFC3401500National Natural Science Foundation of China 82192881National Natural Science Foundation of China 82273931
6 · The paper itself

Abstract

Osteoclasts derived bone marrow monocytes have been documented to modulate bone quality by directly sensing mechanical forces. However, the mechanisms by which osteoclasts perceive and respond to mechanical disturbances remain unclear. Through integrating multi-omics data of bone tissues from hindlimb unloading (HLU) and control mice, it is revealed that glutamine (Gln) catabolism-induced suppression of apoptosis is critical for monocytes sensing and responding to mechanical unloading. Gln uptake is essential for the survival of monocytes under mechanical unloading. Deprivation of Gln or blockade of Gln transporter solute carrier family 1 member 5 (SLC1A5) inhibits bone resorption by enhancing apoptosis of monocytes. Unloading exposure-induced cell survival is mediated by X-linked inhibitor of apoptosis protein (XIAP)/direct IAP binding protein with low pI (Diablo) axis. Upon mechanical unloading XIAP is upregulated, then interacts with Diablo in mitochondrial and promotes the K63-linkage ubiquitylation of Diablo at the K212 site. This sequesters Diablo within the mitochondrial and inhibits its release into the cytosol, ultimately inhibiting cell apoptosis of osteoclasts and the precursors. Clinically, the serum Gln levels are positively correlated with cross linked C-telopeptide of type I collagen (CTX) levels, indicating that serum Gln levels might serve as a potential biomarker for predicting the risk of osteoporosis. Gln-deficient diet, as well as SLC1A5 inhibitor L-γ-Glutamyl-p-nitroanilide (GPNA), effectively preserves bone mass in HLU mice, implicating attractive approaches for combating bone loss induced by weightlessness or disuse.

Indexed as

ApoptosisGlutamineHindlimb SuspensionMonocytesAnimalsBone ResorptionHumansMaleMiceMice, Inbred C57BLMultiomicsOsteoclastsGlutaminebone resorptionglutamineintrinsic apoptosis pathwayK63‐linkage ubiquitylationmechanical unloading

Identifiers

PMID40820799
PMCPMC12622456

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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.