Therapeutic Potential of Targeting the PERK Signaling Pathway in Ischemic Stroke

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-lik...

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Main Authors: Xinyuan Yu (Author), Lihong Dang (Author), Ran Zhang (Author), Wei Yang (Author)
Format: Book
Published: MDPI AG, 2024-03-01T00:00:00Z.
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042 |a dc 
100 1 0 |a Xinyuan Yu  |e author 
700 1 0 |a Lihong Dang  |e author 
700 1 0 |a Ran Zhang  |e author 
700 1 0 |a Wei Yang  |e author 
245 0 0 |a Therapeutic Potential of Targeting the PERK Signaling Pathway in Ischemic Stroke 
260 |b MDPI AG,   |c 2024-03-01T00:00:00Z. 
500 |a 10.3390/ph17030353 
500 |a 1424-8247 
520 |a 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. 
546 |a EN 
690 |a ER stress 
690 |a UPR 
690 |a ischemia 
690 |a autophagy 
690 |a oxidative stress 
690 |a mitochondria 
690 |a Medicine 
690 |a R 
690 |a Pharmacy and materia medica 
690 |a RS1-441 
655 7 |a article  |2 local 
786 0 |n Pharmaceuticals, Vol 17, Iss 3, p 353 (2024) 
787 0 |n https://www.mdpi.com/1424-8247/17/3/353 
787 0 |n https://doaj.org/toc/1424-8247 
856 4 1 |u https://doaj.org/article/add49f68cd664bad91d632a29e6f3bb2  |z Connect to this object online.