Evidence map›Paper›PMID 33824228›Full record

ArticleAging2021

ASIC1 and ASIC3 mediate cellular senescence of human nucleus pulposus mesenchymal stem cells during intervertebral disc degeneration.

Jingyu Ding, Renjie Zhang, Huimin Li, Qiang Ji, Xiaomin Cheng, Rick Francis Thorne, Hubert Hondermarck, Xiaoying Liu, Cailiang Shen

Open access · greenAbstract read
In one paragraph

Article in Aging, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
5.5field-weighted citation impact, top 3% 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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 50 citations in OpenAlex.

  1. Pooled it
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  5. Mechanism of glycolysis-pyrolysis crosstalk driving vicious circle of intervertebral disc degeneration.Apoptosis : an international journal on programmed cell death · 2025
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  9. ASIC1a mediated nucleus pulposus cells pyroptosis and glycolytic crosstalk as a molecular basis for intervertebral disc degeneration.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
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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

9 authors at 4 institutions in 2 countries.

Jingyu DingDepartment of Orthopedics and Spine Surgery, The First Affiliated Hospital, Anhui Medical University, Hefei 230032, Anhui, China.
Renjie ZhangDepartment of Orthopedics and Spine Surgery, The First Affiliated Hospital, Anhui Medical University, Hefei 230032, Anhui, China.
Huimin LiDepartment of Orthopedics and Spine Surgery, The First Affiliated Hospital, Anhui Medical University, Hefei 230032, Anhui, China.
Qiang JiSchool of Life Sciences, Anhui Medical University, Hefei 230032, Anhui, China.
Xiaomin ChengSchool of Life Sciences, Anhui Medical University, Hefei 230032, Anhui, China.
Rick Francis ThorneTranslational Research Institute of Henan Provincial People's Hospital and People's Hospital of Zhengzhou University, Molecular Pathology Centre, Academy of Medical Sciences, Zhengzhou University, Zhengzhou 450053, Henan, China.
Hubert HondermarckSchool of Biomedical Sciences and Pharmacy, University of Newcastle, Callaghan, NSW 2308, Australia.
Xiaoying LiuSchool of Life Sciences, Anhui Medical University, Hefei 230032, Anhui, China.
Cailiang ShenDepartment of Orthopedics and Spine Surgery, The First Affiliated Hospital, Anhui Medical University, Hefei 230032, Anhui, China.
Anhui Medical University · CNFirst Affiliated Hospital of Anhui Medical University · CNHenan Provincial People's Hospital · CNUniversity of Newcastle Australia · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Stem cell approaches have become an attractive therapeutic option for intervertebral disc degeneration (IVDD). Nucleus pulposus mesenchymal stem cells (NP-MSCs) participate in the regeneration and homeostasis of the intervertebral disc (IVD), but the molecular mechanisms governing these processes remain to be elucidated. Acid-sensing ion channels (ASICs) which act as key receptors for extracellular protons in central and peripheral neurons, have been implicated in IVDD where degeneration is associated with reduced microenvironmental pH. Here we show that ASIC1 and ASIC3, but not ASIC2 and ASIC4 are upregulated in human IVDs according to the degree of clinical degeneration. Subjecting IVD-derived NP-MSCs to pH 6.6 culture conditions to mimic pathological IVD changes resulted in decreased cell proliferation that was associated with cell cycle arrest and induction of senescence. Key molecular changes observed were increased expression of p53, p21, p27, p16 and Rb1. Instructively, premature senescence in NP-MSCs could be largely alleviated using ASIC inhibitors, suggesting both ASIC1 and ASIC3 act decisively upstream to activate senescence programming pathways including p53-p21/p27 and p16-Rb1 signaling. These results highlight the potential of ASIC inhibitors as a therapeutic approach for IVDD and broadly define an

Indexed as

Acid Sensing Ion ChannelsAdolescentAdultCells, CulturedCellular SenescenceFemaleHumansIntervertebral DiscIntervertebral Disc DegenerationMaleMesenchymal Stem CellsMiddle AgedNucleus PulposusYoung AdultAcid Sensing Ion ChannelsASIC1 protein, humanASIC3 protein, humanacid sensing ion channels (ASICs)cellular senescenceintervertebral disc degeneration (IVDD)nucleus pulposus mesenchymal stem cells (NP-MSCs)

Identifiers

PMID33824228
PMCPMC8064223
OpenAlexW3147632129

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.