Evidence map›Paper›PMID 36034777›Full record

ArticleFrontiers in pharmacology2022

Melatonin promotes sirtuin 1 expression and inhibits IRE1α-XBP1S-CHOP to reduce endoplasmic reticulum stress-mediated apoptosis in chondrocytes.

Kunpeng Qin, Hao Tang, Yi Ren, Di Yang, Yetian Li, Wei Huang, Yunfeng Wu, Zongsheng Yin

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in pharmacology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing 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

20 citing papers in PubMed.

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  13. Roles of the Caspase-11 Non-Canonical Inflammasome in Rheumatic Diseases.International journal of molecular sciences · 2024
    Review
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  18. Melatonin and bone-related diseases: an updated mechanistic overview of current evidence and future prospects.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2023
    Review
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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

8 authors.

Kunpeng QinDepartment of Orthopaedics, The First Affiliated Hospital of Anhui Medical University, Hefei, China.
Hao TangDepartment of Orthopaedics, The First Affiliated Hospital of Anhui Medical University, Hefei, China.
Yi RenDepartment of Orthopaedics, The First Affiliated Hospital of Anhui Medical University, Hefei, China.
Di YangDepartment of Orthopaedics, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China.
Yetian LiDepartment of Orthopaedics, The First Affiliated Hospital of Anhui Medical University, Hefei, China.
Wei HuangDepartment of Orthopaedics, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China.
Yunfeng WuDepartment of Orthopaedics, The First Affiliated Hospital of Anhui Medical University, Hefei, China.
Zongsheng YinDepartment of Orthopaedics, The First Affiliated Hospital of Anhui Medical University, Hefei, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Osteoarthritis (OA) is the most common chronic disease characterized by a loss of chondrocytes and the degeneration of cartilage. Inflammation plays an important role in the pathogenesis and progression of OA via the activation of the endoplasmic reticulum (ER) stress signaling pathway. In this study, we stimulated human primary chondrocytes with lipopolysaccharide (LPS) to reduce cell viability and induce chondrocyte apoptosis. LPS-stimulated human primary chondrocytes induced ER stress and significantly upregulated the ER chaperone glucose-regulated protein 78 (GRP78) and increased the expression level of C/EBP-homologous protein (CHOP), a key mediator of ER stress--induced apoptosis. Interestingly, melatonin treatment attenuated ER stress-mediated chondrocyte apoptosis. Melatonin inhibited the expression of cleaved caspase-3, cleaved caspase-10, Bax, CHOP, GRP78, cleaved caspase-4, phospho-inositol-requiring enzyme 1α (P-IRE1α), and spliced X-box-binding protein 1 (XBP1S). In an anterior cruciate ligament transection mouse model of OA, melatonin (50 and 150 mg/kg) dose-dependently relieved joint cartilage degeneration and inhibitied of chondrocyte apoptosis. Immunohistochemical analysis indicated that melatonin could promote SIRT1 the expression and inhibit CHOP and cleaved caspase-3 expression in OA mice. In conclusion, our findings demonstrate for the first time that melatonin inhibits the IRE1α-XBP1S-CHOP signaling pathway by promoting the expression of SIRT1 in LPS-treated human chondrocytes and delaying OA progression

Indexed as

apoptosisendoplasmic reticulum stressIRE1α--XBP1S--CHOPmelatoninosteoarthritis

Identifiers

PMID36034777
PMCPMC9404507

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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.