Evidence map›Paper›PMID 40836293›Full record

ArticleJournal of orthopaedic surgery and research2025

ALKBH5 suppresses miR-29a-3p expression, thereby exacerbating the inflammatory response associated with spinal tuberculosis.

Mengqi Zhu, Zhengyong Tao, XingYu Duan, Lijun Feng, Xiaojun Ma, Jiong Wang, ZhiYun Shi, Xu Zhang, NingKui Niu

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Article in Journal of orthopaedic surgery and research, 2025. 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 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

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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

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3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors.

Mengqi Zhu *Department of Orthopedic, General Hospital of Ningxia Medical University, Ningxia Hui Autonomous Region, No.804 Shengli Street, Yinchuan, 750004, China.
Zhengyong Tao *Department of Orthopedic, General Hospital of Ningxia Medical University, Ningxia Hui Autonomous Region, No.804 Shengli Street, Yinchuan, 750004, China.
XingYu DuanDepartment of Orthopedic, General Hospital of Ningxia Medical University, Ningxia Hui Autonomous Region, No.804 Shengli Street, Yinchuan, 750004, China.
Lijun FengDepartment of Orthopedic, General Hospital of Ningxia Medical University, Ningxia Hui Autonomous Region, No.804 Shengli Street, Yinchuan, 750004, China.
Xiaojun MaDepartment of Orthopedic, General Hospital of Ningxia Medical University, Ningxia Hui Autonomous Region, No.804 Shengli Street, Yinchuan, 750004, China.
Jiong WangDepartment of Orthopedic, General Hospital of Ningxia Medical University, Ningxia Hui Autonomous Region, No.804 Shengli Street, Yinchuan, 750004, China.
ZhiYun ShiKey Laboratory of Clinical Pathogenic Microorganisms, General Hospital of Ningxia Medical University, Yinchuan, 750004, Ningxia, China.
Xu ZhangDepartment of Surgery laboratory, Institute of Medical Sciences, General Hospital of Ningxia Medical University, Yinchuan, 750004, Ningxia, China. xuzhang1012@163.com.
NingKui NiuDepartment of Orthopedic, General Hospital of Ningxia Medical University, Ningxia Hui Autonomous Region, No.804 Shengli Street, Yinchuan, 750004, China. niuningkui6743242@163.com.

Funding

National Natural Science Foundation of China No. 82260436
6 · The paper itself

Abstract

backgroundN6-methyladenosine (m6A) is the most common and abundant internal modification in RNA. However, the role of m6A in spinal tuberculosis (STB) remains incompletely elucidated. In our previous study, miRNA-seq was performed on peripheral blood and tissues from STB patients, and miR-29a-3p was identified as differentially expressed in STB patients through screening. In this study, we mainly explored the regulation of miR-29a-3p by ALKB homolog 5 (ALKBH5) in STB.

methodsTissue specimens were obtained from 20 patients with lumbar degenerative disease and 20 patients with STB. The expression levels of ALKBH5 and miR-29a-3p in STB were assessed using qRT-PCR, immunohistochemistry, and immunofluorescence assays. MeRIP analyses were performed to investigate the role of ALKBH5 in regulating the m6A modification of miR-29a-3p. Additionally, Western blot, ELISA, and qRT-PCR techniques were employed to validate the regulatory mechanism of ALKBH5-mediated miR-29a-3p in the inflammatory response associated with STB.

resultsALKBH5 was upregulated in both spinal tuberculosis tissues and cellular models, whereas miR-29a-3p exhibited marked downregulation. Inhibition of miR-29a-3p expression led to increased levels of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-17 A (IL-17 A). Conversely, overexpression of miR-29a-3p effectively suppressed the production of inflammatory factors. Furthermore, ALKBH5 was found to directly target miR-29a-3p and regulate its methylation modification, thereby inhibiting the maturation of miR-29a-3p. Additionally, ALKBH5 suppressed the expression of miR-29a-3p, which in turn promoted the release of inflammatory factors associated with spinal tuberculosis.

Indexed as

AlkB Homolog 5, RNA DemethylaseInflammationMicroRNAsTuberculosis, SpinalAdultAgedFemaleHumansMaleMiddle AgedUp-RegulationALKBH5 protein, humanAlkB Homolog 5, RNA DemethylaseMicroRNAsMIRN29a microRNA, humanALKBH5Inflammatory responsemiR-29a-3pSpinal tuberculosis

Identifiers

PMID40836293
PMCPMC12366370

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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.