Evidence map›Paper›PMID 29533927›Full record

ArticleThe Journal of clinical investigation2018

Transient HIF2A inhibition promotes satellite cell proliferation and muscle regeneration.

Liwei Xie, Amelia Yin, Anna S Nichenko, Aaron M Beedle, Jarrod A Call, Hang Yin

Abstract read
In one paragraph

Article in The Journal of clinical investigation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed, 1 pooled it
–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

43 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
  3. Article
  4. Article
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  6. Article
  7. Article
  8. CORP: In vivo muscle strength-perspectives on the design and interpretation of preclinical animal studies.American journal of physiology. Regulatory, integrative and comparative physiology · 2025
    Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Traumatic Skeletal Muscle Injury and Recovery.Advances in experimental medicine and biology · 2025
    Review
  16. Review
  17. Article
  18. Chronic hypoxia impairs skeletal muscle repair via HIF-2α stabilization.Journal of cachexia, sarcopenia and muscle · 2024
    Article
  19. Article
  20. 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

6 authors.

Liwei XieDepartment of Biochemistry and Molecular Biology.
Amelia YinDepartment of Biochemistry and Molecular Biology.
Anna S NichenkoDepartment of Kinesiology, The University of Georgia, Athens, Georgia, USA.
Aaron M BeedleDepartment of Pharmaceutical Sciences, Binghamton University-SUNY, Binghamton, New York, USA.
Jarrod A CallDepartment of Kinesiology, The University of Georgia, Athens, Georgia, USA.
Hang YinDepartment of Biochemistry and Molecular Biology.

Funding

Impacts of hypoxia and hypoxia-induced factors on skeletal muscle repair and muscle stem cellsR01AR070178 · NIAMS · UNIVERSITY OF GEORGIA · PI YIN, HANG · 2016 to 2020
$1.6M
NIAMS NIH HHS R01 AR070178
6 · The paper itself

Abstract

The remarkable regeneration capability of skeletal muscle depends on the coordinated proliferation and differentiation of satellite cells (SCs). The self-renewal of SCs is critical for long-term maintenance of muscle regeneration potential. Hypoxia profoundly affects the proliferation, differentiation, and self-renewal of cultured myoblasts. However, the physiological relevance of hypoxia and hypoxia signaling in SCs in vivo remains largely unknown. Here, we demonstrate that SCs are in an intrinsic hypoxic state in vivo and express hypoxia-inducible factor 2A (HIF2A). HIF2A promotes the stemness and long-term homeostatic maintenance of SCs by maintaining their quiescence, increasing their self-renewal, and blocking their myogenic differentiation. HIF2A stabilization in SCs cultured under normoxia augments their engraftment potential in regenerative muscle. Conversely, HIF2A ablation leads to the depletion of SCs and their consequent regenerative failure in the long-term. In contrast, transient pharmacological inhibition of HIF2A accelerates muscle regeneration by increasing SC proliferation and differentiation. Mechanistically, HIF2A induces the quiescence and self-renewal of SCs by binding the promoter of the Spry1 gene and activating Spry1 expression. These findings suggest that HIF2A is a pivotal mediator of hypoxia signaling in SCs and may be therapeutically targeted to improve muscle regeneration.

Indexed as

Cell ProliferationRegenerationSignal TransductionAnimalsBasic Helix-Loop-Helix ProteinsCell DifferentiationCell HypoxiaEndothelial PAS Domain-Containing Protein 1MiceMice, TransgenicMuscle DevelopmentMuscle, SkeletalSatellite Cells, Skeletal MuscleBasic Helix-Loop-Helix ProteinsEndothelial PAS Domain-Containing Protein 1Adult stem cellsMuscle BiologySkeletal muscleStem cells

Identifiers

PMID29533927
PMCPMC5983316

What OpenQuestion holds

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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.