Evidence map›Paper›PMID 40713978›Full record

ArticleThe American journal of pathology2025

miR-204-5p Mitigates Disc Degeneration via SKI-Mediated Modulation of Apoptotic Signaling and Matrix Remodeling in Nucleus Pulposus.

Rui Ran, Chao-Yang Gong, Zuo-Long Wu, Shun-Bai Zhang, Kai Zhang, Wen-Ming Zhou, Wei Song, Hao Dong, Yong-Qiang Shi, Kai-Sheng Zhou and 1 more

Abstract read
In one paragraph

Article in The American journal of pathology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

11 authors.

Rui RanThe Second Hospital & Clinical Medical School, Lanzhou University, Lanzhou, China; Orthopaedics Key Laboratory of Gansu Province, Lanzhou, China.
Chao-Yang GongThe Second Hospital & Clinical Medical School, Lanzhou University, Lanzhou, China; Orthopaedics Key Laboratory of Gansu Province, Lanzhou, China.
Zuo-Long WuThe Second Hospital & Clinical Medical School, Lanzhou University, Lanzhou, China; Orthopaedics Key Laboratory of Gansu Province, Lanzhou, China.
Shun-Bai ZhangThe Second Hospital & Clinical Medical School, Lanzhou University, Lanzhou, China; Orthopaedics Key Laboratory of Gansu Province, Lanzhou, China.
Kai ZhangThe Second Hospital & Clinical Medical School, Lanzhou University, Lanzhou, China; Orthopaedics Key Laboratory of Gansu Province, Lanzhou, China.
Wen-Ming ZhouThe Second Hospital & Clinical Medical School, Lanzhou University, Lanzhou, China; Orthopaedics Key Laboratory of Gansu Province, Lanzhou, China.
Wei SongThe Second Hospital & Clinical Medical School, Lanzhou University, Lanzhou, China; Orthopaedics Key Laboratory of Gansu Province, Lanzhou, China.
Hao DongThe Second Hospital & Clinical Medical School, Lanzhou University, Lanzhou, China; Orthopaedics Key Laboratory of Gansu Province, Lanzhou, China.
Yong-Qiang ShiThe Second Hospital & Clinical Medical School, Lanzhou University, Lanzhou, China; Orthopaedics Key Laboratory of Gansu Province, Lanzhou, China.
Kai-Sheng ZhouThe Second Hospital & Clinical Medical School, Lanzhou University, Lanzhou, China; Orthopaedics Key Laboratory of Gansu Province, Lanzhou, China.
Hai-Hong ZhangThe Second Hospital & Clinical Medical School, Lanzhou University, Lanzhou, China; Orthopaedics Key Laboratory of Gansu Province, Lanzhou, China. Electronic address: 549990342@qq.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dysregulation of nucleus pulposus cells (NPCs) is a critical contributor to intervertebral disc degeneration (IDD). One characteristic of degenerated discs is the increased apoptosis of NPCs and the substantial degradation of the extracellular matrix (ECM). This study identified significantly reduced miR-204-5p levels in IDD tissues. Using lipopolysaccharide (LPS)-treated rat NPCs, miR-204-5p overexpression was found to suppress apoptosis, reduce ECM degradation, and enhance ECM synthesis. Mechanistically, SKI was identified as a direct target of miR-204-5p, with its expression markedly elevated in IDD tissues. Functional assays revealed that modulating SKI expression (overexpression or knockdown) influenced LPS-induced apoptosis, ECM synthesis, and degradation in NPCs. Notably, SKI overexpression exacerbated LPS-induced damage and counteracted the protective effects of miR-204-5p. Importantly, intradiscal delivery of agomiR-204-5p effectively alleviated IDD progression in vivo. Overall, these results emphasize the pivotal role of miR-204-5p in mitigating IDD by targeting SKI, thereby regulating NPC apoptosis and ECM homeostasis. The miR-204-5p/SKI axis thus presents a promising therapeutic avenue for treating IDD.

Indexed as

ApoptosisDNA-Binding ProteinsExtracellular MatrixIntervertebral Disc DegenerationMicroRNAsNucleus PulposusProto-Oncogene ProteinsAnimalsHumansMaleRatsRats, Sprague-DawleySignal TransductionDNA-Binding ProteinsMicroRNAsMIRN204 microRNA, humanProto-Oncogene ProteinsSKI protein, human

Identifiers

PMID40713978
PMCPMC12597460

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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.