Evidence map›Paper›PMID 42821156›Full record

ReviewMolecular neurobiology2026

HTR3A Receptor Signaling in Human Disease: From Bioelectrical Regulation to Therapeutic Targeting.

Ghasem Ahangari, Fatemeh Abedini, Shadi Ghaemi

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In one paragraph

Review in Molecular neurobiology, 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

3 authors.

Ghasem AhangariDepartment of Medical Genetics, National Institute of Genetic Engineering and Biotechnology, Tehran, Iran. ghah@nigeb.ac.ir.ORCID http://orcid.org/0000-0002-4259-7672
Fatemeh AbediniDepartment of Medical Genetics, National Institute of Genetic Engineering and Biotechnology, Tehran, Iran.ORCID http://orcid.org/0000-0001-7679-1070
Shadi GhaemiDepartment of Medical Genetics, National Institute of Genetic Engineering and Biotechnology, Tehran, Iran.ORCID http://orcid.org/0009-0005-9033-2416

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The 5-hydroxytryptamine receptor 3A (HTR3A) is the principal subunit of the 5-HT3 receptor and the only ionotropic member of the serotonin receptor family, mediating rapid cation influx and membrane depolarization following stimulation by serotonin. Beyond its established role in neurotransmission, growing evidence indicates that HTR3A functions as a critical regulator of bioelectrical signaling, influencing calcium homeostasis, neuronal excitability, immune responses, and diverse cellular processes implicated in human disease. This narrative review provides a comprehensive overview of the molecular structure, physiological functions, and pathological significance of HTR3A, with particular emphasis on its role in integrating bioelectrical mechanisms across multiple organ systems. Current evidence linking HTR3A dysregulation to cancer, neurological and psychiatric disorders, gastrointestinal diseases, inflammatory conditions, and pain is critically evaluated, highlighting shared electrophysiological pathways that may underlie these seemingly distinct pathologies. We further discuss the therapeutic potential of HTR3A-targeted interventions, including the repurposing of clinically approved 5-HT3 receptor antagonists, and examine emerging opportunities for biomarker development and precision medicine. Although substantial progress has been made in elucidating the biological functions of HTR3A, significant challenges remain regarding its context-dependent roles, mechanistic complexity, and clinical translation. By integrating molecular, electrophysiological, and translational evidence, this review proposes a unifying framework in which HTR3A-mediated bioelectrical signaling represents a common mechanistic axis linking diverse human diseases, thereby providing new perspectives for future mechanistic investigations and targeted therapeutic strategies.

Indexed as

DiseaseElectrophysiological PhenomenaMolecular Targeted TherapyReceptors, Serotonin, 5-HT3Signal TransductionAnimalsHumansSerotonin 5-HT3 Receptor AntagonistsHTR3A protein, humanReceptors, Serotonin, 5-HT3Serotonin 5-HT3 Receptor Antagonists5-hydroxytryptamine type 3 A (HTR3A)Bioelectrical signalingCancerNeurodegenerative diseases

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Registered trials

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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.