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The Role of Inflammasome Complex in Ischemia-Reperfusion Injury Publisher Pubmed



Mohamadi Y1 ; Mousavi M1 ; Khanbabaei H2 ; Salarinia R3 ; Javankiani S1 ; Hassanzadeh G1 ; Momeni F4
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Authors Affiliations
  1. 1. Department of Anatomy, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
  2. 2. Radiobiology Laboratory, Medical Physics Department, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
  3. 3. Department of Medical Biotechnology and Molecular Sciences, School of Medicine, North Khorasan University of Medical Sciences, Bojnurd, Iran
  4. 4. Health research institute, Faculty of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran

Source: Journal of Cellular Biochemistry Published:2023


Abstract

Ischemia-reperfusion injury refers to a temporary interruption of blood flow in a tissue. Restoration of blood flow initiates the inflammation in tissue causing ischemic damage through the activation of a multiprotein complex termed inflammasome. The complex contains a receptor, mainly a member of nucleotide oligomerization domain–like receptors, that receives danger signals. The receptor is oligomerized as a response to danger signals and then the apoptosis-associated speck-like protein containing a caspase recruitment domain and procaspase protein are added to the oligomerized receptors to form the inflammasome complex. In the next step, the isolated procaspase is converted into an active caspase molecule that initiates the inflammation through the release of interleukin-1β and interleukin-18. The inflammasome has an important role in the pathogenesis of ischemia-reperfusion injury in different tissues. Here, we summarized the role of inflammasome in the pathogenesis of ischemia-reperfusion of brain, liver, kidney, and heart. Moreover, we highlighted the expression of inflammasome components, the mechanisms involved in activation of the complex, and its inhibition as an optimistic therapeutic technique in ischemia-reperfusion injuries. © 2018 Wiley Periodicals, Inc.
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