Evidence map›Paper›PMID 25482050›Full record

ReviewMolecular neurobiology2016

Crosstalk Between Endoplasmic Reticulum Stress, Oxidative Stress, and Autophagy: Potential Therapeutic Targets for Acute CNS Injuries.

Venkata Prasuja Nakka, Phanithi Prakash-Babu, Raghu Vemuganti

Abstract readReview
In one paragraph

Review in Molecular neurobiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 139 papers.

0numbers the graph read from it
0cells of the map it votes in
139citing papers in PubMed
7.9field-weighted citation impact, top 2% of its field
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

139 citing papers in PubMed, 251 citations in OpenAlex.

  1. Article
  2. Review
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  4. Article
  5. Intravenous miR-30c therapy confers dual neurovascular protection and improves long-term recovery after ischemic stroke.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026
    Article
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  20. Lentinan progress in inflammatory diseases and tumor diseases.European journal of medical research · 2024
    Review

79 more citing papers are in PubMed but not listed here.

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 at 2 institutions in 2 countries.

Venkata Prasuja NakkaDepartment of Neurological Surgery, School of Medicine and Public Health, University of Wisconsin, Madison, WI, 53792, USA.
Phanithi Prakash-BabuDepartment of Biotechnology & Bioinformatics, School of Life sciences, University of Hyderabad, Hyderabad, India.
Raghu VemugantiDepartment of Neurological Surgery, School of Medicine and Public Health, University of Wisconsin, Madison, WI, 53792, USA. vemuganti@neurosurgery.wisc.edu.
University of Wisconsin–Madison · USUniversity of Hyderabad · IN

Funding

Synergy of ER stress and oxidative stress after TBIR21NS082957 · NINDS · UNIVERSITY OF WISCONSIN-MADISON · PI VEMUGANTI, RAGHU · 2013 to 2014
$412k
Combo therapy to curtail oxidative stress after TBIR03NS083007 · NINDS · UNIVERSITY OF WISCONSIN-MADISON · PI VEMUGANTI, RAGHU · 2013 to 2014
$150k
NINDS NIH HHS R03 NS083007NINDS NIH HHS R21 NS082957
6 · The paper itself

Abstract

Endoplasmic reticulum (ER) stress induces a variety of neuronal cell death pathways that play a critical role in the pathophysiology of stroke. ER stress occurs when unfolded/misfolded proteins accumulate and the folding capacity of ER chaperones exceeds the capacity of ER lumen to facilitate their disposal. As a consequence, a complex set of signaling pathways will be induced that transmit from ER to cytosol and nucleus to compensate damage and to restore the normal cellular homeostasis, collectively known as unfolded protein response (UPR). However, failure of UPR due to severe or prolonged stress leads to cell death. Following acute CNS injuries, chronic disturbances in protein folding and oxidative stress prolong ER stress leading to sustained ER dysfunction and neuronal cell death. While ER stress responses have been well studied after stroke, there is an emerging need to study the association of ER stress with other cell pathways that exacerbate neuronal death after an injury. In this review, we summarize the current understanding of the role for ER stress in acute brain injuries, highlighting the diverse molecular mechanisms associated with ER stress and its relation to oxidative stress and autophagy. We also discussed the existing and developing therapeutic options aimed to reduce ER stress to protect the CNS after acute injuries.

Indexed as

Drug Delivery SystemsAnimalsAutophagyCentral Nervous System DiseasesEndoplasmic Reticulum StressHumansNeuroprotective AgentsOxidative StressSignal TransductionNeuroprotective AgentsAcute CNS injuryAutophagyCrosstalkER stressOxidative stress

Identifiers

PMID25482050
PMCPMC4461562
OpenAlexW2043275103

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.