OSCR

AhR inhibition promotes axon regeneration via a stress-growth switch.

A correction to this paper has been published: the notice, 42706336, from Europe PMC.

Overview

Authors: Dalia Halawani1,2, Yiqun Wang1,3, Jiaxi Li1, Daniel Halperin1, Haofei Ni1, Molly Estill1, Aarthi Ramakrishnan1, Li Shen1, Arthur Sefiani4, Cédric G Geoffroy4,5, Roland H Friedel1,6, Hongyan Zou1,6
ORCID iDs: Dalia Halawani, Yiqun Wang, Daniel Halperin, Haofei Ni, Li Shen, Arthur Sefiani, Cédric G Geoffroy, Roland H Friedel, Hongyan Zou
  1. Nash Family Department of Neuroscience, Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, NY USA
  2. Present Address: Center for Pharmacology, Institute II, Faculty of Medicine, University Hospital Cologne, Cologne, Germany
  3. Present Address: Sports Medicine Center, Honghui Hospital, Xi’an Jiaotong University, Xi’an, China
  4. Department of Neuroscience and Experimental Therapeutics, College of Medicine, Texas A&M University, College Station, TX USA
  5. Wolfson Sensory, Pain and Regeneration Centre (SPaRC), King’s College London, London, UK
  6. Department of Neurosurgery, Icahn School of Medicine at Mount Sinai, New York, NY USA
Institutions: University Hospital Cologne (Germany); Icahn School of Medicine at Mount Sinai (United States); Xi'an Honghui Hospital (China); Xi'an Jiaotong University (China); Texas A&M University (United States); King's College London (United Kingdom)
Journal: Nature, volume 653, issue 8116, pages 1119-1129
Dates: received 13 September 2023; accepted 18 February 2026; published online 1 April 2026; in print 2026
Type: Research article · Language: English
License: CC BY-NC-ND
Identifiers: DOI 10.1038/s41586-026-10295-z · PMID 41922778 · PMCID PMC13216071 · OpenAlex W7147612840
Open access: hybrid, a free copy (OpenAlex)
Status: data only
Categories: genetics / omics (modality), mouse (organism), other condition (population), cellular / molecular (subfield)
Methods: Statistics, Evoked potentials, fMRI & imaging, Smoothing, state filtering, decompositions
Keywords: Neuroscience, Genetics of the nervous system
MeSH: Axons*, Basic Helix-Loop-Helix Proteins*, Nerve Regeneration*, Receptors, Aryl Hydrocarbon*, Stress, Physiological*, Animals, DNA Methylation, Female, Ganglia, Spinal, Hypoxia-Inducible Factor 1, alpha Subunit, Integrated Stress Response, Ligands, Mice, Peripheral Nerve Injuries, Proteotoxic Stress, Signal Transduction, Spinal Cord Injuries (* major topic)
Topic: Nerve injury and regeneration (Cellular and Molecular Neuroscience, Neuroscience), according to OpenAlex
Funding: NINDS NIH HHS (R01 NS127442, R21 NS131834, R01 NS128101)
Citations: cited by 3 papers (Europe PMC); 89 references in the paper
Notices: A correction to this paper has been published (42706336, from Europe PMC)

Abstract

The abstract is not reproduced here: the paper's license (CC BY-NC-ND) does not allow it. Read it in the paper, at the publisher or on Europe PMC.

Code

The paper links to its data, not to its authors' code: see the Data section.

Code availability statement

The paper has a code availability statement. Its license (CC BY-NC-ND) does not allow reproducing it here; in short, from what the harvester recognized in it:

  • no repository, dataset or request procedure was recognized in it

Read it in the paper: doi.org/10.1038/s41586-026-10295-z.

Tracing map

A tracing map links a paper to the code its authors published: this paper has none, so it has no map.

Data

Datasets cited

Data availability statement

The paper has a data availability statement. Its license (CC BY-NC-ND) does not allow reproducing it here; in short, from what the harvester recognized in it:

Read it in the paper: doi.org/10.1038/s41586-026-10295-z.

Versions

The history of this record: each version stored by the harvester or made by a correction of its authors or of the maintainers of its code, and what changed in its facts. The texts of the paper (its abstract, its availability statements) are not part of it; versions that changed only those are not listed.

Version 2, 28 September 2026

  • Publisher: n/a → Nature Portfolio

Version 1, 28 September 2026: the first record

Recorded: type, language, journal, volume, issue, pages, dates, 12 authors, 2 keywords, 17 MeSH terms, 1 funder, 88 references, 1 integrity notice.

Cite

This paper

Halawani, D., Wang, Y., Li, J., Halperin, D., Ni, H., Estill, M., Ramakrishnan, A., Shen, L., Sefiani, A., Geoffroy, C. G., Friedel, R. H., & Zou, H. (2026). AhR inhibition promotes axon regeneration via a stress-growth switch. Nature, 653(8116), 1119-1129. https://doi.org/10.1038/s41586-026-10295-z

BibTeX

@article{halawani2026ahr,
author = {Halawani, Dalia and Wang, Yiqun and Li, Jiaxi and Halperin, Daniel and Ni, Haofei and Estill, Molly and Ramakrishnan, Aarthi and Shen, Li and Sefiani, Arthur and Geoffroy, Cédric G and Friedel, Roland H and Zou, Hongyan},
title = {{AhR inhibition promotes axon regeneration via a stress-growth switch}},
journal = {Nature},
year = {2026},
month = apr,
volume = {653},
number = {8116},
pages = {1119--1129},
publisher = {Nature Portfolio},
issn = {0028-0836},
doi = {10.1038/s41586-026-10295-z},
url = {https://doi.org/10.1038/s41586-026-10295-z},
pmid = {41922778},
pmcid = {PMC13216071}
}

RIS

TY - JOUR
AU - Halawani, Dalia
AU - Wang, Yiqun
AU - Li, Jiaxi
AU - Halperin, Daniel
AU - Ni, Haofei
AU - Estill, Molly
AU - Ramakrishnan, Aarthi
AU - Shen, Li
AU - Sefiani, Arthur
AU - Geoffroy, Cédric G
AU - Friedel, Roland H
AU - Zou, Hongyan
TI - AhR inhibition promotes axon regeneration via a stress-growth switch
T2 - Nature
J2 - Nature
PY - 2026
DA - 2026/04/01
VL - 653
IS - 8116
SP - 1119
EP - 1129
SN - 0028-0836
PB - Nature Portfolio
DO - 10.1038/s41586-026-10295-z
UR - https://doi.org/10.1038/s41586-026-10295-z
LA - en
ER -

CSL-JSON

{
"id": "10.1038/s41586-026-10295-z",
"type": "article-journal",
"title": "AhR inhibition promotes axon regeneration via a stress-growth switch",
"container-title": "Nature",
"author": [
{
"family": "Halawani",
"given": "Dalia"
},
{
"family": "Wang",
"given": "Yiqun"
},
{
"family": "Li",
"given": "Jiaxi"
},
{
"family": "Halperin",
"given": "Daniel"
},
{
"family": "Ni",
"given": "Haofei"
},
{
"family": "Estill",
"given": "Molly"
},
{
"family": "Ramakrishnan",
"given": "Aarthi"
},
{
"family": "Shen",
"given": "Li"
},
{
"family": "Sefiani",
"given": "Arthur"
},
{
"family": "Geoffroy",
"given": "Cédric G"
},
{
"family": "Friedel",
"given": "Roland H"
},
{
"family": "Zou",
"given": "Hongyan"
}
],
"container-title-short": "Nature",
"volume": "653",
"issue": "8116",
"page": "1119-1129",
"DOI": "10.1038/s41586-026-10295-z",
"PMID": "41922778",
"PMCID": "PMC13216071",
"ISSN": "0028-0836",
"publisher": "Nature Portfolio",
"URL": "https://doi.org/10.1038/s41586-026-10295-z",
"language": "en",
"issued": {
"date-parts": [
[
2026,
4,
1
]
]
}
}

Similar papers

The papers with a page that share the most with this one: the tools found in their code, their categories, datasets, cited references and authors, the rarest counting most.

[1] doi:10.1126/sciadv.adw4136 [code]
Directional guidance to orient Schwann cell alignment in nerve regeneration requires Plexin-B1.
Journal: Science advances
In common: mouse, cellular / molecular, 9 references, 5 authors
[2] doi:10.1073/pnas.2537017123
Distinct cell type-specific mechanisms underlie cognitive dysfunction during persistent integrated stress response activation.
Journal: Proceedings of the National Academy of Sciences of the United States of America
In common: genetics / omics, mouse, cellular / molecular, 4 references
[3] doi:10.1016/j.cell.2026.05.047 [code]
An emergent disease-associated motor neuron state precedes cell death in ALS.
Journal: Cell
In common: genetics / omics, other condition, mouse, 1 other category, 3 references
[4] doi:10.1038/s41467-026-71803-3 [code]
Charting the transition from in vitro gliogenesis to the in vivo maturation of human glial progenitor cells transplanted into the hypomyelinated mouse brain.
Journal: Nature communications
In common: genetics / omics, mouse, cellular / molecular, 3 references
[5] doi:10.1172/jci192328
Skin-resident Langerhans cells drive neuropathic pain via chemokine-dependent neuron-immune communication.
Journal: The Journal of clinical investigation
In common: other condition, mouse, cellular / molecular, 3 references
[6] doi:10.1016/j.celrep.2026.117408
NAT10-dependent N<sup>4</sup>-acetylcytidine reprograms R-loops and promotes cancer stem cell growth.
Journal: Cell reports
In common: other condition, mouse, cellular / molecular, 3 references
[7] doi:10.1186/s12964-026-02920-1
ARNT2 repression disrupts neuronal identity and promotes glioblastoma growth.
Journal: Cell communication and signaling : CCS
In common: other condition, mouse, cellular / molecular, 2 references
[8] doi:10.1038/s41467-026-73505-2 [code]
Light- and chemical-induced ciliary signaling governs dorsal/ventral regionalization of human telencephalic organoids.
Journal: Nature communications
In common: 4 references
[9] doi:10.3390/ijms27083598
Decoding Prognostic Signatures in Brain Metastatic Non-Small-Cell Lung Cancer via Integrated Multi-Omics and Network Analysis.
Journal: International journal of molecular sciences
In common: genetics / omics, other condition, 3 references
[10] doi:10.1210/endocr/bqag087
A single-nucleus multiomic study of preoptic area cells in prepubertal control vs prenatally androgenized female mice.
Journal: Endocrinology
In common: genetics / omics, mouse, 3 references

Contribute

The authors of this paper can claim it, correct its record and validate its tracing map, and the maintainers of its code (its owner, or a public member of its organization) correct what it says of their repository; anyone signed in can ask for its removal. Every request goes to OSCR's own machine, which answers it; your account page follows them.

Sign in with ORCID to claim this paper as one of its authors, correct its record or validate its tracing map: when the paper's metadata lists your ORCID iD, you are recognized at once. Maintainers of its code: sign in with GitHub, then claim the repository on your account page.

Request its removal

To ask OSCR to remove this record, the copies of its authors' scripts or its tracing map, use the removal request page: signed in, you say who you are, what to remove and why, then review and confirm the request. Published rules decide every request (how).

Discussion, reproductions, activity

Discussion: questions and error reports about this paper and its code, from signed-in readers and its authors. It opens with sign-in.

Reproductions: reports from readers who ran the authors' code: what they reproduced, with which environment, commit and data. It opens with sign-in.

Activity: what happens around this paper: new versions of its record, its map's validation, discussions and reproductions. It opens with sign-in.