Evidence map›Paper›PMID 40251566›Full record

ArticleJournal of neuroinflammation2025

A molecular brain atlas reveals cellular shifts during the repair phase of stroke.

Rebecca Z Weber, Beatriz Achón Buil, Nora H Rentsch, Allison Bosworth, Mingzi Zhang, Kassandra Kisler, Christian Tackenberg, Ruslan Rust

Abstract read
In one paragraph

Article in Journal of neuroinflammation, 2025. 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
–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

19 citing papers in PubMed.

  1. Article
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  10. "Time Is Brain" - for Cell Therapies.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Review
  11. Article
  12. Review
  13. Article
  14. Article
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  17. The blood-brain barrier: a help and a hindrance.Brain : a journal of neurology · 2025
    Review
  18. Review
  19. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors.

Rebecca Z WeberInstitute for Regenerative Medicine, University of Zurich, Schlieren, 8952, Switzerland.
Beatriz Achón BuilInstitute for Regenerative Medicine, University of Zurich, Schlieren, 8952, Switzerland.
Nora H RentschInstitute for Regenerative Medicine, University of Zurich, Schlieren, 8952, Switzerland.
Allison BosworthDepartment of Physiology and Neuroscience, University of Southern California, Los Angeles, CA, 90033, USA.
Mingzi ZhangDepartment of Physiology and Neuroscience, University of Southern California, Los Angeles, CA, 90033, USA.
Kassandra KislerDepartment of Physiology and Neuroscience, University of Southern California, Los Angeles, CA, 90033, USA.
Christian TackenbergInstitute for Regenerative Medicine, University of Zurich, Schlieren, 8952, Switzerland.
Ruslan RustDepartment of Physiology and Neuroscience, University of Southern California, Los Angeles, CA, 90033, USA. rrust@usc.edu.ORCID http://orcid.org/0000-0003-3376-3453

Funding

Activated protein C mechanisms of brain white matter protection and new therapies for brain white matter ischemic injuryR01NS117827 · NINDS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI MACK, WILLIAM J · 2020 to 2025
$3.4M
NINDS NIH HHS R01 NS117827
6 · The paper itself

Abstract

Ischemic stroke triggers a cascade of pathological events that affect multiple cell types and often lead to incomplete functional recovery. Despite advances in single-cell technologies, the molecular and cellular responses that contribute to long-term post-stroke impairment remain poorly understood. To gain better insight into the underlying mechanisms, we generated a single-cell transcriptomic atlas from distinct brain regions using a mouse model of permanent focal ischemia at one month post-injury. Our findings reveal cell- and region-specific changes within the stroke-injured and peri-infarct brain tissue. For instance, GABAergic and glutamatergic neurons exhibited upregulated genes in signaling pathways involved in axon guidance and synaptic plasticity, and downregulated pathways associated with aerobic metabolism. Using cell-cell communication analysis, we identified increased strength in predicted interactions within stroke tissue among both neural and non-neural cells via signaling pathways such as those involving collagen, protein tyrosine phosphatase receptor, neuronal growth regulator, laminin, and several cell adhesion molecules. Furthermore, we found a strong correlation between mouse transcriptome responses after stroke and those observed in human nonfatal brain stroke lesions. Common molecular features were linked to inflammatory responses, extracellular matrix organization, and angiogenesis. Our findings provide a detailed resource for advancing our molecular understanding of stroke pathology and for discovering therapeutic targets in the repair phase of stroke recovery.

Indexed as

BrainStrokeAnimalsHumansMaleMiceMice, Inbred C57BLNeuronsRecovery of FunctionSingle-Cell AnalysisTranscriptome

Identifiers

PMID40251566
PMCPMC12008922

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.