Evidence map›Paper›PMID 31313490›Full record

ArticleAging cell2019

Hsp90β interacts with MDM2 to suppress p53-dependent senescence during skeletal muscle regeneration.

Min Yi He, Shui Bo Xu, Zi Hao Qu, Yue Mei Guo, Xiao Ceng Liu, Xiao Xia Cong, Jian Feng Wang, Boon Chuan Low, Li Li, Qiang Wu and 5 more

Open access · goldAbstract read
In one paragraph

Article in Aging cell, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

23 citing papers in PubMed, 49 citations in OpenAlex.

  1. HSP90β as a potential prognostic biomarker in urothelial carcinoma: insights from NF-κB, IL-8, and heat-shock protein expression.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
    Article
  2. Review
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  5. Chaperone Proteins: The Rising Players in Muscle Atrophy.Journal of cachexia, sarcopenia and muscle · 2025
    Review
  6. Article
  7. Article
  8. PARP1 Promotes Heart Regeneration and Cardiomyocyte Proliferation.International journal of biological sciences · 2024
    Article
  9. Article
  10. Article
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  12. Review
  13. Extracellular HSP90α promotes cellular senescence by modulating TGF-β signaling in pulmonary fibrosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022
    Article
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  15. Review
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  19. Review
  20. In vivo analysis of γH2AX+ cells in skeletal muscle from aged and obese humans.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020
    Article
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 at 5 institutions in 3 countries.

Min Yi HeDepartment of Biochemistry and Molecular Biology, Department of Orthopaedic Surgery of the Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Shui Bo XuDepartment of Biochemistry and Molecular Biology, Department of Orthopaedic Surgery of the Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Zi Hao QuDepartment of Biochemistry and Molecular Biology, Department of Orthopaedic Surgery of the Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Yue Mei GuoDepartment of Biochemistry and Molecular Biology, Department of Orthopaedic Surgery of the Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Xiao Ceng LiuDepartment of Biochemistry and Molecular Biology, Department of Orthopaedic Surgery of the Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Xiao Xia CongDepartment of Biochemistry and Molecular Biology, Department of Orthopaedic Surgery of the Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Jian Feng WangDepartment of Respiratory Medicine, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Boon Chuan LowMechanobiology Institute, Department of Biological Sciences, National University of Singapore, Singapore.
Li LiInstitute of Aging Research, Hangzhou Normal University, Hangzhou, China.
Qiang WuThe State Key Laboratory of Quality Research in Chinese Medicine, Macau University of Science and Technology, Macau, China.
Peng LinDepartment of Biochemistry and Molecular Biology, Department of Orthopaedic Surgery of the Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Shi Gui YanDepartment of Biochemistry and Molecular Biology, Department of Orthopaedic Surgery of the Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Zhang BaoDepartment of Respiratory Medicine, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Yi Ting ZhouDepartment of Biochemistry and Molecular Biology, Department of Orthopaedic Surgery of the Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.ORCID 0000-0003-4543-3099
Li Ling ZhengDepartment of Biochemistry and Molecular Biology, Department of Orthopaedic Surgery of the Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Second Affiliated Hospital of Zhejiang University · CNFirst Affiliated Hospital Zhejiang University · CNHangzhou Normal University · CNMacau University of Science and Technology · MONational University of Singapore · SG

Funding

International Science & Technology Cooperation Program of ChinaKey Scientific and Technological Innovation Team of Zhejiang Province 2013TD11Ministry of Science and Technology of PRC 2015DFG32130National Natural Science Foundation of China 31571402National Natural Science Foundation of China 31671417Science and Technology Commission of Zhejiang Province LY13C070002
6 · The paper itself

Abstract

Cellular senescence plays both beneficial and detrimental roles in embryonic development and tissue regeneration, while the underlying mechanism remains elusive. Recent studies disclosed the emerging roles of heat-shock proteins in regulating muscle regeneration and homeostasis. Here, we found that Hsp90β, but not Hsp90α isoform, was significantly upregulated during muscle regeneration. RNA-seq analysis disclosed a transcriptional elevation of p21 in Hsp90β-depleted myoblasts, which is due to the upregulation of p53. Moreover, knockdown of Hsp90β in myoblasts resulted in p53-dependent cellular senescence. In contrast to the notion that Hsp90 interacts with and protects mutant p53 in cancer, Hsp90β preferentially bound to wild-type p53 and modulated its degradation via a proteasome-dependent manner. Moreover, Hsp90β interacted with MDM2, the chief E3 ligase of p53, to regulate the stability of p53. In line with these in vitro studies, the expression level of p53-p21 axis was negatively correlated with Hsp90β in aged mice muscle. Consistently, administration of 17-AAG, a Hsp90 inhibitor under clinical trial, impaired muscle regeneration by enhancing injury-induced senescence in vivo. Taken together, our finding revealed a previously unappreciated role of Hsp90β in regulating p53 stability to suppress senescence both in vitro and in vivo.

Indexed as

Cellular SenescenceAnimalsCell LineHSP90 Heat-Shock ProteinsMiceMuscle, SkeletalProto-Oncogene Proteins c-mdm2Tumor Suppressor Protein p53HSP90 Heat-Shock ProteinsMdm2 protein, mouseProto-Oncogene Proteins c-mdm2Tumor Suppressor Protein p53cellular senescenceheat-shock proteinHsp90βMDM2muscle regenerationp53senescenceskeletal muscle

Identifiers

PMID31313490
PMCPMC6718578
OpenAlexW2960912787

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.