ReviewPharmaceuticals (Basel, Switzerland)2024
Therapeutic Potential of Targeting the PERK Signaling Pathway in Ischemic Stroke.
Review in Pharmaceuticals (Basel, Switzerland), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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.
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.
Who cites it
13 citing papers in PubMed, 14 citations in OpenAlex.
- ATF4 orchestrates cancer hallmarks: Stress adaptation, metabolic reprogramming and immune suppression.iScience · 2026Review
- Cell-Penetrating Peptide-Mediated Modulation of Endoplasmic Reticulum Stress: A Bioengineered and Translational Approach.ACS pharmacology & translational science · 2026Review
- Targeting endoplasmic reticulum stress for neuroprotection in ischemia-reperfusion injury: mechanisms and therapeutic approaches.Molecular biology reports · 2026Review
- Baicalin Alleviates LPS-Induced Apoptosis of Periodontal Ligament Cells Via Inhibiting Endoplasmic Reticulum Stress.International dental journal · 2026Article
- Ischemic stroke neuroprotection revisited: translational barriers and a phase-resolved, biomarker-anchored framework.Archives of pharmacal research · 2026Review
- RNA-binding protein ELAVL1 modulates WDR36 to inhibit p53 pathway and reduce calcium overload in retinal cells under acute pressure elevation.Open life sciences · 2026Article
- Activation of ATF6 Signaling Confers Long-Term Beneficial Effects in Young and Aged Mice After Permanent Stroke.Translational stroke research · 2025Article
- A Small-Molecule Activator of Sarco/Endoplasmic Reticulum CaACS pharmacology & translational science · 2025Article
- Enhanced membrane protein production in HEK293T cells viaBiomolecules & biomedicine · 2025Article
- Environmental adversity, endoplasmic reticulum stress, and neurogenesis.Neurotoxicology · 2025Review
- Exploring Research Trends and Mechanisms: Maternal Diabetes and Neural Tube Defects (1991-2023).Journal of multidisciplinary healthcare · 2025Article
- Maximizing ISRIB Potential Requires Addressing Specificity, Long-term Safety, and Disease-specific Considerations.Current medicinal chemistry · 2025Review
- Exploring Endocannabinoid System: Unveiling New Roles in Modulating ER Stress.Antioxidants (Basel, Switzerland) · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Many pathologic states can lead to the accumulation of unfolded/misfolded proteins in cells. This causes endoplasmic reticulum (ER) stress and triggers the unfolded protein response (UPR), which encompasses three main adaptive branches. One of these UPR branches is mediated by protein kinase RNA-like ER kinase (PERK), an ER stress sensor. The primary consequence of PERK activation is the suppression of global protein synthesis, which reduces ER workload and facilitates the recovery of ER function. Ischemic stroke induces ER stress and activates the UPR. Studies have demonstrated the involvement of the PERK pathway in stroke pathophysiology; however, its role in stroke outcomes requires further clarification. Importantly, considering mounting evidence that supports the therapeutic potential of the PERK pathway in aging-related cognitive decline and neurodegenerative diseases, this pathway may represent a promising therapeutic target in stroke. Therefore, in this review, our aim is to discuss the current understanding of PERK in ischemic stroke, and to summarize pharmacologic tools for translational stroke research that targets PERK and its associated pathways.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.