Cerebral ischemia is a pathological condition resulting from the cessation or reduction of blood supply to the cerebral arteries. Neurological deficits that are clinically relevant can arise as a result of brain damage. The etiology of stroke is multifaceted and intricate, with the inflammatory response being a crucial component that warrants significant attention. Following a cerebrovascular accident, the levels of interleukin-1 beta and interleukin-18 within the central nervous system escalate due to the activation of the nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing 3 inflammasome. The inflammation is aggravated by the subsequent occurrence of pyroptosis. The mechanisms that activate the NLRP3 inflammasome pyroptosis signaling pathway axis are described in this article. In addition, we go over how pyroptosis interacts with other processes for regulated cell death. In addition, specific NLRP3 inflammasome pathway inhibitors are identified, which offer new approaches to preventing ischemic brain injury.
Keywords: Inflammation; Ischemic stroke; NLRP3 inflammasome; NLRP3 inflammasome inhibitor; Pyroptosis.
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