Evidence map›Paper›PMID 37804406›Full record

ArticleInflammation2024

Suppression of IRF9 Promotes Osteoclast Differentiation by Decreased Ferroptosis via STAT3 Activation.

Chao Lan, Xuan Zhou, Ximei Shen, Youfen Lin, Xiaoyuan Chen, Jiebin Lin, Yongze Zhang, Lifeng Zheng, Sunjie Yan

Erratum issuedAbstract read
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In one paragraph

Article in Inflammation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
2.5field-weighted citation impact, top 11% 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

15 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 2 institutions in 1 country.

Chao LanDepartment of Endocrinology, The First Affiliated Hospital, Fujian Medical University, Fuzhou, 350005, China.
Xuan ZhouDepartment of Endocrinology, The First Affiliated Hospital, Fujian Medical University, Fuzhou, 350005, China.
Ximei ShenDepartment of Endocrinology, The First Affiliated Hospital, Fujian Medical University, Fuzhou, 350005, China.
Youfen LinDepartment of Endocrinology, The First Affiliated Hospital, Fujian Medical University, Fuzhou, 350005, China.
Xiaoyuan ChenDepartment of Endocrinology, The First Affiliated Hospital, Fujian Medical University, Fuzhou, 350005, China.
Jiebin LinDepartment of Endocrinology, The First Affiliated Hospital, Fujian Medical University, Fuzhou, 350005, China.
Yongze ZhangDepartment of Endocrinology, The First Affiliated Hospital, Fujian Medical University, Fuzhou, 350005, China.
Lifeng ZhengOrthopedics Department, The First Affiliated Hospital of Fujian Medical University, Fuzhou, 350005, Fujian, China.
Sunjie YanDepartment of Endocrinology, The First Affiliated Hospital, Fujian Medical University, Fuzhou, 350005, China. fjyansunjie@163.com.
First Affiliated Hospital of Fujian Medical University · CNFujian Medical University · CN

Funding

Scientific and Technological Major Special Project of Fujian Provincial Health Commission No.2021ZD01004the Natural Science Foundation of Fujian Province No. 2020J02052the Startup Fund for Scientifc Research, Fujian Medical University No.2021QH2033
6 · The paper itself

Abstract

Osteoporosis is a chronic disease that endangers the health of the elderly. Inhibiting osteoclast hyperactivity is a key aspect of osteoporosis prevention and treatment. Several studies have shown that interferon regulatory factor 9 (IRF9) not only regulates innate and adaptive immune responses but also plays an important role in inflammation, antiviral response, and cell development. However, the exact role of IRF9 in osteoclasts has not been reported. To elucidate the role of IRF9 in osteoclast differentiation, we established the ovariectomized mouse model of postmenopausal osteoporosis and found that IRF9 expression was reduced in ovariectomized mice with overactive osteoclasts. Furthermore, knockdown of IRF9 expression enhanced osteoclast differentiation in vitro. Using RNA sequencing, we identified that the differentially expressed genes enriched by IRF9 knockdown were related to ferroptosis. We observed that IRF9 knockdown promoted osteoclast differentiation via decreased ferroptosis in vitro and further verified that IRF9 knockdown reduced ferroptosis by activating signal transducer and activator of transcription 3 (STAT3) to promote osteoclastogenesis. In conclusion, we identified an essential role of IRF9 in the regulation of osteoclastogenesis in osteoporosis and its underlying mechanism.

Indexed as

Bone ResorptionFerroptosisOsteoporosisAgedAnimalsCell DifferentiationHumansInterferon-Stimulated Gene Factor 3, gamma SubunitMiceOsteoclastsOsteogenesisRANK LigandSignal TransductionSTAT3 Transcription FactorInterferon-Stimulated Gene Factor 3, gamma SubunitIRF9 protein, humanIsgf3g protein, mouseRANK LigandSTAT3 protein, humanSTAT3 Transcription FactorFerroptosisIRF9OsteoclastRNA sequencingSTAT3

Identifiers

PMID37804406
OpenAlexW4387426121

What OpenQuestion holds

Textmetadata
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.