Evidence map›Paper›PMID 37492931›Full record

ArticleEMBO reports2023

TRIM71 reactivation enhances the mitotic and hair cell-forming potential of cochlear supporting cells.

Xiao-Jun Li, Charles Morgan, Prathamesh T Nadar-Ponniah, Waldemar Kolanus, Angelika Doetzlhofer

Open access · greenAbstract read
In one paragraph

Article in EMBO reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

6 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Review
  3. The RNA-binding protein TRIM71 is essential for hearing in humans and mice and times auditory sensory organ development.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  4. Article
  5. Article
  6. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 2 countries.

Xiao-Jun LiThe Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD, USA.ORCID 0000-0001-7345-2364
Charles MorganThe Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD, USA.ORCID 0000-0002-8766-0954
Prathamesh T Nadar-PonniahThe Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD, USA.ORCID 0000-0002-1087-9069
Waldemar KolanusMolecular Immunology and Cell Biology, Life & Medical Sciences Institute (LIMES), University of Bonn, Bonn, Germany.ORCID 0000-0003-1325-9444
Angelika DoetzlhoferThe Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD, USA.ORCID 0000-0002-7424-2112
Johns Hopkins University · USUniversity of Bonn · DE

Funding

The function of LIN28B and follistatin in supporting cell reprogramming and hair cell regeneration in the murine cochleaR01DC019359 · NIDCD · JOHNS HOPKINS UNIVERSITY · PI ANGELIKA DOETZLHOFER · 2022 to 2026
$2.5M
The role of supporting cell de-differentiation in cochlear hair cell regenerationF31DC020882 · NIDCD · JOHNS HOPKINS UNIVERSITY · PI MORGAN, CHARLES · 2022 to 2024
$143k
NIDCD NIH HHS F31 DC020882NIDCD NIH HHS R01 DC019359
6 · The paper itself

Abstract

Cochlear hair cell loss is a leading cause of deafness in humans. Neighboring supporting cells have some capacity to regenerate hair cells. However, their regenerative potential sharply declines as supporting cells undergo maturation (postnatal day 5 in mice). We recently reported that reactivation of the RNA-binding protein LIN28B restores the hair cell-regenerative potential of P5 cochlear supporting cells. Here, we identify the LIN28B target Trim71 as a novel and equally potent enhancer of supporting cell plasticity. TRIM71 is a critical regulator of stem cell behavior and cell reprogramming; however, its role in cell regeneration is poorly understood. Employing an organoid-based assay, we show that TRIM71 re-expression increases the mitotic and hair cell-forming potential of P5 cochlear supporting cells by facilitating their de-differentiation into progenitor-like cells. Our mechanistic work indicates that TRIM71's RNA-binding activity is essential for such ability, and our transcriptomic analysis identifies gene modules that are linked to TRIM71 and LIN28B-mediated supporting cell reprogramming. Furthermore, our study uncovers that the TRIM71-LIN28B target Hmga2 is essential for supporting cell self-renewal and hair cell formation.

Indexed as

CochleaHair Cells, AuditoryAnimalsCell DifferentiationGene Expression ProfilingHumansMiceStem CellsTranscription FactorsTripartite Motif ProteinsUbiquitin-Protein LigasesLIN-41 protein, mouseTranscription FactorsTRIM71 protein, humanTripartite Motif ProteinsUbiquitin-Protein Ligasescochleahair cell regenerationLin28bsupporting cell reprogrammingTrim71

Identifiers

PMID37492931
PMCPMC10481673
OpenAlexW4385264527

What OpenQuestion holds

Textmetadata
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.