The NLRP3 inflammasome: a potential therapeutic target for traumatic brain injury
Saifudeen Ismael1
Heba A.Ahmed1
Tusita Adris1
Kehkashan Parveen2
Parth Thakor1
Tauheed Ishrat3
1.Department of Anatomy and Neurobiology,University of Tennessee Health Science Center,Memphis,TN,USA2.Department of Biochemistry,Hamdard University,New Delhi,India3.Department of Anatomy and Neurobiology,University of Tennessee Health Science Center,Memphis,TN,USA;Neuroscience Institute,University of Tennessee Health Science Center,Memphis,TN,USA
摘要：Although the precise mechanisms contributing to secondary brain injury following traumatic brain injury are complex and obscure, a number of studies have demonstrated that inflammatory responses are an obvious and early feature in the pathogenesis of traumatic brain injury. Inflammasomes are multiprotein complexes that prompt the stimulation of caspase-1 and subsequently induce the maturation and secretion of proinflammatory cytokines, such as interleukin-1β and interleukin-18. These cytokines play a pivotal role in facilitating innate immune responses and inflammation. Among various inflammasome complexes, the NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome is the best characterized, a crucial role for NLRP3 has been demonstrated in various brain diseases, including traumatic brain injury. Several recent studies have revealed the contribution of NLRP3 inflammasome in identifying cellular damage and stimulating inflammatory responses to aseptic tissue injury after traumatic brain injury. Even more important, blocking or inhibiting the activation of the NLRP3 inflammasome may have substantial potential to salvage tissue damage during traumatic brain injury. In this review, we summarize recently described mechanisms that are involved in the activation and regulation of the NLRP3 inflammasome. Moreover, we review the recent investigations on the contribution of the NLRP3 inflammasome in the pathophysiology of TBI, and current advances and challenges in potential NLRP3-targeted therapies. A significant contribution of NLRP3 inflammasome activation to traumatic brain injury implies that therapeutic approaches focused on targeting specific inflammasome components could significantly improve the traumatic brain injury outcomes.
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论文发表日期：2021-01-28
在线出版日期：2025-08-15（本平台首次上网日期，不代表文献的发表时间）
页数：9( 49-57 )
英文信息