Evidence map›Paper›PMID 40395988›Full record

ReviewAutophagy reports2025

The role of autophagy in ischemic brain injury.

Emily Osterli, Yujung Park, Kurt Hu, Gary Kasof, Thorsten Wiederhold, Chunli Liu, Bingren Hu

Abstract readReview
In one paragraph

Review in Autophagy reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. White matter injury after brain ischemia.Experimental neurology · 2026
    Review
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

7 authors.

Emily OsterliDepartments of Emergency Medicine and Neurosciences, University of California San Diego, La Jolla, CA, USA.
Yujung ParkDepartments of Emergency Medicine and Neurosciences, University of California San Diego, La Jolla, CA, USA.
Kurt HuDepartment of Medicine, Division of Pulmonary and Critical Care, Medical College of Wisconsin, Milwaukee, WI, USA.
Gary KasofDepartments of Product Design and Strategy and Antibody Protein Technology, Cell Signaling Technology, Danvers, MA, USA.
Thorsten WiederholdDepartments of Product Design and Strategy and Antibody Protein Technology, Cell Signaling Technology, Danvers, MA, USA.
Chunli LiuDepartments of Emergency Medicine and Neurosciences, University of California San Diego, La Jolla, CA, USA.
Bingren HuDepartments of Emergency Medicine and Neurosciences, University of California San Diego, La Jolla, CA, USA.

Funding

Testing Cerebroprotective Interventions with Rodent Ischemic Stroke ModelsU01NS130557 · NINDS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI HU, BINGREN · 2023 to 2025
$1.8M
Dysfunctional organelle-specific autophagy leads to brain ischemia-reperfusion injuryR01NS134895 · NINDS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI Bingren Hu · 2024 to 2026
$1.8M
Novel anti-NPC aggregation strategy against brain ischemia-reperfusion injuryR01NS097875 · NINDS · UNIVERSITY OF MARYLAND BALTIMORE · PI HU, BINGREN · 2017 to 2021
$1.7M
Change in NSF ATPase activity Leads to Brain Ischemia Reperfusion InjuryR01NS102815 · NINDS · UNIVERSITY OF MARYLAND BALTIMORE · PI HU, BINGREN · 2018 to 2023
$1.7M
The Role of Lysosomal Membrane Permeabilization and Cathepsin B Release in Stroke Brain InjuryR01NS129553 · NINDS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI Bingren Hu · 2023 to 2026
$1.5M
BLRD VA I01 BX005814NINDS NIH HHS R01 NS097875NINDS NIH HHS R01 NS102815NINDS NIH HHS R01 NS129553NINDS NIH HHS R01 NS134895NINDS NIH HHS U01 NS130557
6 · The paper itself

Abstract

Ischemic brain injury occurs in many clinical settings, including stroke, cardiac arrest, hypovolemic shock, cardiac surgery, cerebral edema, and cerebral vasospasm. Decades of work have revealed many important mechanisms related to ischemic brain injury. However, there remain significant gaps in the scientific knowledge to reconcile many ischemic brain injury events. Brain ischemia leads to protein misfolding and aggregation, and damages almost all types of subcellular organelles including mitochondria, endoplasmic reticulum, Golgi apparatus, lysosomes, etc. Irreparably damaged organelles and insoluble protein aggregates are normally removed by autophagy. The build-up of common autophagic components, such as LC3, p62, and ubiquitinated proteins, are generally observed in brain tissue samples in animal models of both global and focal brain ischemia, but the interpretation of the role of these autophagy-related changes in ischemic brain injury in the literature has been controversial. Many pathological events or mechanisms underlying dysfunctional autophagy after brain ischemia remain unknown. This review aims to provide an update of the current knowledge and future research directions regarding the critical role of dysfunctional autophagy in ischemic brain injury.

Indexed as

Amphisomesautophagosomeautophagy relatedcathepsinslate endosomelysosomesmicrotubule-associated protein 1A/1B–light chain 3N-ethylmaleimide sensitive factor proteinsequestosome 1soluble NSF attachment proteins receptor

Identifiers

PMID40395988
PMCPMC11980474

What OpenQuestion 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 OpenQuestion graph.