Evidence map›Paper›PMID 40714837›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025

PIEZO1-GPX4 Axis Mediates Mechanical Stress-Induced Vertebral Growth Plate Dysplasia via Ferroptosis Activation.

Fei Chen, Fushuai Peng, Shuqing Chen, Yukun Du, Jianyi Li, Yuanyuan Fan, Zichen Cui, Guanghui Gu, Han Zhang, Zhensong Jiang and 5 more

Abstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing 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

13 citing papers in PubMed.

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  5. The therapeutic potential of Piezo1 channel-mediated ferroptosis and its inhibitor.Apoptosis : an international journal on programmed cell death · 2026
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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

15 authors.

Fei ChenDepartment of Spinal Surgery, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, 266071, China.
Fushuai PengDepartment of Spinal Surgery, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, 266071, China.
Shuqing ChenDepartment of Spinal Surgery, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, 266071, China.
Yukun DuDepartment of Spinal Surgery, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, 266071, China.
Jianyi LiDepartment of Spinal Surgery, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, 266071, China.
Yuanyuan FanShandong Public Health Clinical Center, Shandong University, Jinan, Shandong, 250013, China.
Zichen CuiDepartment of Spinal Surgery, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, 266071, China.
Guanghui GuDepartment of Spinal Surgery, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, 266071, China.
Han ZhangDepartment of Spinal Surgery, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, 266071, China.
Zhensong JiangDepartment of Spine Surgery, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, 250021, China.
Guodong WangDepartment of Spine Surgery, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, 250021, China.
Xingzhi JingDepartment of Spine Surgery, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, 250021, China.
Jun DongDepartment of Spine Surgery, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, 250021, China.
Tao LiDepartment of Spine Surgery, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, 250021, China.ORCID https://orcid.org/0000-0002-9165-3239
Yongming XiDepartment of Spinal Surgery, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, 266071, China.ORCID https://orcid.org/0000-0002-2921-0699

Funding

Qingdao Technology-Benefiting-People Program 23-2-8-amjk-9-nshTaishan Scholar Project of Shandong Province, China ts20190985Taishan Scholars Program of Shandong Province tstp20250511Young Elite Sponsorship Program of Shandong Provincial Medical Association 2023_GJ_0085
6 · The paper itself

Abstract

Current scientific consensus acknowledges mechanical stress, particularly compressive loading, as a critical contributor to the pathogenesis of vertebral growth plate disorders (VGPD), though the precise molecular mechanisms remain incompletely understood. This study establishes PIEZO1 as a mechanosensitive ion channel central to compressive stress responses. These findings demonstrate that PIEZO1 upregulation disrupts GPX4 signaling, thereby amplifying ferroptosis in vertebral growth plate chondrocytes and accelerating pathological ossification. Pharmacological inhibition of PIEZO1 effectively attenuated iron overload, mitigated oxidative stress, and suppressed mechanical stress-induced ferroptosis cascades. Notably, both conditional PIEZO1 knockout models (Col2a1-CreERT; Piezo1

Indexed as

FerroptosisGrowth PlateIon ChannelsPhospholipid Hydroperoxide Glutathione PeroxidaseAnimalsChondrocytesDisease Models, AnimalHumansMiceMice, KnockoutOsteogenesisSignal TransductionStress, MechanicalIon ChannelsPhospholipid Hydroperoxide Glutathione PeroxidasePiezo1 protein, mousechondrocytesferroptosismechanical stressPIEZO1scoliosis

Identifiers

PMID40714837
PMCPMC12533149

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.