Evidence map›Paper›PMID 38330941›Full record

ArticleAmerican journal of human genetics2024

The cells of the sensory epithelium, and not the stria vascularis, are the main cochlear cells related to the genetic pathogenesis of age-related hearing loss.

Mai Eshel, Beatrice Milon, Ronna Hertzano, Ran Elkon

Open access · bronzeAbstract read
In one paragraph

Article in American journal of human genetics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
6.1field-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

8 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. TNFAIP8L2 maintains hair cell function and regulates age-related hearing loss via mTORC1 signaling.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Article
  6. Review
  7. Pharmacological Approaches to Hearing Loss.Pharmacological reviews · 2024
    Review
  8. 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

4 authors at 2 institutions in 2 countries.

Mai EshelDepartment of Human Molecular Genetics and Biochemistry, School of Medicine, Tel Aviv University, Tel Aviv, Israel.
Beatrice MilonNeurotology Branch, NIDCD, National Institutes of Health, Bethesda, MD, USA.
Ronna HertzanoNeurotology Branch, NIDCD, National Institutes of Health, Bethesda, MD, USA. Electronic address: ronna.hertzano@nih.gov.
Ran ElkonDepartment of Human Molecular Genetics and Biochemistry, School of Medicine, Tel Aviv University, Tel Aviv, Israel. Electronic address: ranel@tauex.tau.ac.il.
National Institutes of Health · USTel Aviv University · IL

Funding

UNIVERSITY OF MARYLAND GREENEBAUM CANCER CENTERSUPPORT GRANTP30CA134274 · NCI · UNIVERSITY OF MARYLAND BALTIMORE · PI FEYRUZ VIRGILIA RASSOOL · 2008 to 2026
$51.0M
Multi-Omic and Functional Analyses for Hearing Preservation and RestorationZIADC000094 · NIDCD · NATIONAL INSTITUTE ON DEAFNESS AND OTHER COMMUNICATION DISORDERS · PI HERTZANO, RONNA · 2023 to 2025
$10.3M
The gEAR portal - Advancing Data Sharing, Analysis and Discovery for Hearing and Balance ResearchR01DC019370 · NIDCD · UNIVERSITY OF MARYLAND BALTIMORE · PI MAHURKAR, ANUP · 2021 to 2022
$1.5M
TEMPORAL ACOUSTIC ANALYSIS IN LATERAL LEMNISCAL NUCLEIF32DC000094 · NIDCD · DUKE UNIVERSITY · PI HUFFMAN, RUSSELL F · 1992 to 1995
–
NCI NIH HHS P30 CA134274NIDCD NIH HHS DC000094NIDCD NIH HHS F32 DC000094NIDCD NIH HHS R01 DC019370
6 · The paper itself

Abstract

Age-related hearing loss (ARHL) is a major health concern among the elderly population. It is hoped that increasing our understanding of its underlying pathophysiological processes will lead to the development of novel therapies. Recent genome-wide association studies (GWASs) discovered a few dozen genetic variants in association with elevated risk for ARHL. Integrated analysis of GWAS results and transcriptomics data is a powerful approach for elucidating specific cell types that are involved in disease pathogenesis. Intriguingly, recent studies that applied such bioinformatics approaches to ARHL resulted in disagreeing findings as for the key cell types that are most strongly linked to the genetic pathogenesis of ARHL. These conflicting studies pointed either to cochlear sensory epithelial or to stria vascularis cells as the cell types most prominently involved in the genetic basis of ARHL. Seeking to resolve this discrepancy, we integrated the analysis of four ARHL GWAS datasets with four independent inner-ear single-cell RNA-sequencing datasets. Our analysis clearly points to the cochlear sensory epithelial cells as the key cells for the genetic predisposition to ARHL. We also explain the limitation of the bioinformatics analysis performed by previous studies that led to missing the enrichment for ARHL GWAS signal in sensory epithelial cells. Collectively, we show that cochlear epithelial cells, not stria vascularis cells, are the main inner-ear cells related to the genetic pathogenesis of ARHL.

Indexed as

PresbycusisStria VascularisAgedCochleaEpitheliumGenome-Wide Association StudyHumansage-related hearing lossARHLcochleagenetics of age-related hearing lossGWASsingle-cell RNA-seq

Identifiers

PMID38330941
PMCPMC10940011
OpenAlexW4391598528

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.