Evidence map›Paper›PMID 31493568›Full record

ReviewHearing research2019

Cochlear histopathology in human genetic hearing loss: State of the science and future prospects.

Krishna Bommakanti, Janani S Iyer, Konstantina M Stankovic

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Hearing research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.1field-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

19 citing papers in PubMed, 39 citations in OpenAlex.

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  16. Missense Variant of Endoplasmic Reticulum Region ofBioMed research international · 2021
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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

3 authors at 3 institutions in 1 country.

Krishna BommakantiDepartment of Otolaryngology, Harvard Medical School, Boston, MA, USA; Eaton Peabody Laboratories and Department of Otolaryngology, Massachusetts Eye and Ear, Boston, MA, USA; University of California San Diego School of Medicine, San Diego, CA, USA.
Janani S IyerDepartment of Otolaryngology, Harvard Medical School, Boston, MA, USA; Eaton Peabody Laboratories and Department of Otolaryngology, Massachusetts Eye and Ear, Boston, MA, USA; Program in Speech and Hearing Bioscience and Technology, Harvard Medical School, Boston, MA, USA; Wellman Center for Photomedicine, Massachusetts General Hospital, Boston, MA, USA.
Konstantina M StankovicDepartment of Otolaryngology, Harvard Medical School, Boston, MA, USA; Eaton Peabody Laboratories and Department of Otolaryngology, Massachusetts Eye and Ear, Boston, MA, USA; Program in Speech and Hearing Bioscience and Technology, Harvard Medical School, Boston, MA, USA; Harvard Program in Therapeutic Science, Harvard Medical School, Boston, MA, USA. Electronic address: konstantina_stankovic@meei.harvard.edu.
Harvard University · USMassachusetts General Hospital · USUniversity of California, San Diego · US

Funding

Mechanisms of sensorineural hearing loss: secreted factorsR01DC015824 · NIDCD · STANFORD UNIVERSITY · PI STANKOVIC, KONSTANTINA M · 2016 to 2020
$2.2M
NIDCD NIH HHS R01 DC015824
6 · The paper itself

Abstract

Sensorineural hearing loss (SNHL) is an extraordinarily common disability, affecting 466 million people across the globe. Half of these incidents are attributed to genetic mutations that disrupt the structure and function of the cochlea. The human cochlea's interior cannot be imaged or biopsied without damaging hearing; thus, everything known about the morphologic correlates of hereditary human deafness comes from histopathologic studies conducted in either cadaveric human temporal bone specimens or animal models of genetic deafness. The purpose of the present review is to a) summarize the findings from all published histopathologic studies conducted in human temporal bones with known SNHL-causing genetic mutations, and b) compare the reported phenotypes of human vs. mouse SNHL caused by the same genetic mutation. The fact that human temporal bone histopathologic analysis has been reported for only 22 of the nearly 200 identified deafness-causing genes suggests a great need for alternative and improved techniques for studying human hereditary deafness; in light of this, the present review concludes with a summary of promising future directions, specifically in the fields of high resolution cochlear imaging, intracochlear fluid biopsy, and gene therapy.

Indexed as

MutationAnimalsCochleaDisease Models, AnimalGenetic Predisposition to DiseaseGenetic TherapyHearingHearing Loss, SensorineuralHumansMice, Mutant StrainsPhenotypeSpecies SpecificityHearing lossHistopathologyTemporal bone

Identifiers

PMID31493568
PMCPMC6778517
OpenAlexW2969698119

What Socratic holds

Textmetadata
LicenceTDM
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 Socratic graph.