Evidence map›Paper›PMID 40064756›Full record

ArticleApoptosis : an international journal on programmed cell death2025

Melatonin attenuates inflammatory bone loss by alleviating mitophagy and lactate production.

Zexin Lin, Yuan Gu, Yingsong Liu, Zilin Chen, Shuai Fang, Zhuan Wang, Zixian Liu, Qingrong Lin, Yanjun Hu, Nan Jiang and 2 more

Abstract read
PubMed Publisher
In one paragraph

Article in Apoptosis : an international journal on programmed cell death, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing 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

9 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.

Zexin Lin *Department of Orthopaedics, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Yuan Gu *Department of Orthopaedics, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Yingsong Liu *Huizhou First People's Hospital, Huizhou, China.
Zilin ChenDepartment of Orthopaedics, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Shuai FangTrauma Center, Department of Orthopaedic Trauma, The Second Affiliated Hospital of Hengyang Medical College, South China University, Hengyang, China.
Zhuan WangDepartment of Orthopaedics, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Zixian LiuThe Second Hospital & Clinical Medical School, Lanzhou University, Lanzhou, China.
Qingrong LinDepartment of Orthopaedics, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Yanjun HuDepartment of Orthopaedics, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Nan JiangDepartment of Trauma Emergency Center, Ganzhou Hospital-Nanfang Hospital, Southern Medical University, Ganzhou, China. hnxyjn@smu.edu.cn.
Bin YuDepartment of Orthopaedics, Nanfang Hospital, Southern Medical University, Guangzhou, China. yubin@smu.edu.cn.
Guanqiao LiuDepartment of Orthopaedics, Nanfang Hospital, Southern Medical University, Guangzhou, China. lgq92324@smu.edu.cn.

Funding

Ganzhou City Science and Technology Plan Project GZ2024YLJ036Guangdong Basic and Applied Basic Research Foundation 2023A1515140162Guangzhou Science and Technology Project 2025A04J4182Jiangxi Provincial Natural Science Foundation 20244BAB28035National Natural Science Foundation of China 82201732
6 · The paper itself

Abstract

Mitochondrial homeostasis plays a major role in the progression of chronic inflammatory bone loss which has a complex pathogenesis with unsatisfactory therapeutic efficiency. Recently, melatonin has been shown to recipient mitochondrial function and bone formation. However, the effects and underlying molecular mechanism of melatonin in chronic inflammatory bone loss remain unclear. Here, we reported that melatonin ameliorated lipopolysaccharide (LPS)-induced inflammatory bone loss by improving osteogenesis. We found that melatonin rescued LPS-induced mitochondrial dysfunction and metabolic reprogramming in osteoblasts, resulting in reduced osteogenesis impairment. Mechanistically, melatonin inhibited mitochondrial reactive oxygen species (mtROS) production by suppressing LPS-induced mitophagy, which attenuated the activation of the mtROS/HIF-1α/pyruvate dehydrogenase kinase 1 (PDK1) axis. Moreover, melatonin restored pyruvate dehydrogenase (PDH) activity by inhibiting phosphorylation of PDH through the mtROS/HIF-1α/PDK1 axis and eventually downregulated lactate production. These findings indicate the therapeutic effects of melatonin against chronic inflammatory bone loss and demonstrated a potential treatment strategy against inflammatory osteogenic disorders through regulating mitochondrial dysfunction and metabolic reprogramming.

Indexed as

InflammationLactic AcidMelatoninMitophagyAnimalsHumansHypoxia-Inducible Factor 1, alpha SubunitLipopolysaccharidesMaleMiceMice, Inbred C57BLMitochondriaOsteoblastsOsteogenesisPyruvate Dehydrogenase Acetyl-Transferring KinaseReactive Oxygen SpeciesHif1a protein, mouseHypoxia-Inducible Factor 1, alpha SubunitLactic AcidLipopolysaccharidesMelatoninPyruvate Dehydrogenase Acetyl-Transferring KinaseReactive Oxygen SpeciesInflammatiory bone lossLactateMelatoninMitochondrial reactive oxygen speciesMitophagy

Identifiers

PMID40064756

What OpenQuestion holds

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Registered trials

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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.