Evidence map›Paper›PMID 42307737›Full record

ReviewHNO2026

[Cell and gene therapies in Menière's disease: perspectives for a slowly progressive inner ear disease].

Valentin Fankhauser, Judith S Kempfle

Abstract readEnglish AbstractReview
PubMed Publisher
In one paragraph

Review in HNO, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

2 authors.

Valentin FankhauserKlinik für Ohren‑, Nasen‑, Hals- und Gesichtschirurgie, Universitätsspital Zürich, Zürich, Schweiz.
Judith S KempfleUMass Chan Medical School, Worcester, MA, Massachusetts Eye and Ear, Harvard Medical School, Boston, MA, USA. Judith_kempfle@meei.harvard.edu.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Menière's disease (MD) is classically understood as a pressure-related disease of the inner ear; however, new histopathologic and imaging findings call for reassessment of this model. The current article focuses on new aspects of MD pathophysiology and derives innovative causal treatment approaches for the future based on cell and gene therapy. The recent differentiation between two biologically distinct endotypes (hypoplastic vs. degenerative) shifts the therapeutic focus from purely symptomic pressure reduction toward targeted modulation of epithelial function and regeneration. Building upon this, the article discusses new target structures beyond sensory hair cells, including epithelial cells of the endolymphatic sac and the stria vascularis as well as the ion and water transport mechanisms that are vital for pH regulation and endolymph homeostasis. Focus is also laid on novel, more precise application techniques for cell and gene therapies in the vestibular system that enable tissue-sparing deposition of therapeutic substances in the cochlea, vestibular organs, and stria vascularis. At the molecular level, modern gene therapy strategies are highlighted, complemented by a discussion of new preclinical studies on vestibular hair cell regeneration. Overall, the present article positions MD-for the first time-as an explicit candidate for precision medicine-based combined treatment concepts integrating gene modulation, epithelial repair, and sensory regeneration to offer realistic perspectives for disease-modifying or potentially causal therapy.

Indexed as

Genetic TherapyMeniere DiseaseAnimalsHumansRegenerationStria VascularisCochleaEndolymphPerilymphStria vascularisVestibular regeneration

Identifiers

What Socratic 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 Socratic graph.