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Related Concept Videos

Necrosis01:16

Necrosis

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Necrosis is considered as an “accidental” or unexpected form of cell death that ends in cell lysis. The first noticeable mention of “necrosis” was in 1859 when Rudolf Virchow used this term to describe advanced tissue breakdown in his compilation titled “Cell Pathology”.
Morphological Manifestations of Necrosis
Necrotic cells show different types of morphological appearance depending on the type of tissue and infection. In coagulative necrosis, cells become...
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Evaluating Cell Death Signaling by Immunofluorescence in a Rat Model of Ischemic Stroke
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Evaluating Cell Death Signaling by Immunofluorescence in a Rat Model of Ischemic Stroke

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Regulated necrosis pathways: a potential target for ischemic stroke.

Kaidi Ren1,2,3, Jinyan Pei4, Yuanyuan Guo1,2,3

  • 1Department of Pharmacy, The First Affiliated Hospital of Zhengzhou University, No. 1 Jianshe Dong Road, ErQi District, Zhengzhou 450052, China.

Burns & Trauma
|November 29, 2023
PubMed
Summary

Ischemic stroke causes significant neuronal death via regulated necrosis pathways like necroptosis and ferroptosis. Targeting these pathways offers a promising strategy for neuronal survival and regeneration in stroke patients.

Keywords:
FerroptosisIschemic strokeNecroptosisOncosisPathanatosPyroptosismPTP-mediated necrosis

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Pathology

Background:

  • Ischemic stroke is a leading cause of death globally, with outcomes heavily influenced by neuronal death in the infarct region.
  • Neuronal injury in stroke occurs through regulated pathways (apoptosis, autophagy) and non-regulated necrosis.
  • Regulated necrosis, a non-apoptotic cell death pathway, is increasingly recognized for its role in ischemic stroke.

Purpose of the Study:

  • To review the molecular mechanisms of various regulated necrosis pathways in ischemic stroke.
  • To explore the interactions and crosstalk among different regulated necrosis types.
  • To highlight the therapeutic potential of targeting regulated necrosis for stroke treatment.

Main Methods:

  • Literature review of studies on regulated necrosis in ischemic stroke.
  • Analysis of molecular signaling cascades involved in cell death pathways.
  • Examination of preclinical and clinical data on targeting regulated necrosis.

Main Results:

  • Identified key regulated necrosis pathways including necroptosis, pyroptosis, ferroptosis, and others.
  • Detailed the molecular mechanisms and signaling crosstalk among these pathways.
  • Demonstrated the contribution of regulated necrosis to ischemia- and reperfusion-induced neuronal injury.

Conclusions:

  • Regulated necrosis pathways are critical contributors to neuronal death in ischemic stroke.
  • Understanding the interplay between these pathways is essential for developing effective therapies.
  • Targeting regulated necrosis pharmacologically or genetically presents a viable strategy for enhancing neuronal survival and promoting regeneration after stroke.