Singh Desh Deepak
Amity Institute of Biotechnology, Amity University Rajasthan Jaipur 303002 India
RSC Med Chem. 2025 May 13. doi: 10.1039/d5md00167f.
Drug-induced toxicity is an important issue in clinical medicine, which typically results in organ dysfunction and adverse health consequences. The family of NOD-like receptors (NLRs) includes intracellular proteins involved in recognizing pathogens and triggering innate immune responses, including the activation of the NLRP3 inflammasome. The NLRP3 (nucleotide-binding oligomerization domain-like receptor family, pyrin domain-containing 3) inflammasome is a critical component for both innate and adaptive immune responses and has been implicated in various drug-induced toxicities, including hepatic, renal, and cardiovascular diseases. The unusual activation of the NLRP3 inflammasome causes the release of pro-inflammatory cytokines, such as IL-1β and IL-18, which can lead to more damage to tissues. Targeting NLRP3 inflammasome is a potential therapeutic endeavour for suppressing drug-induced toxicity. This review provides insights into the mechanism, drug-induced organ toxicity, therapeutic strategies, and prospective therapeutic approaches of the NLRP3 inflammasome and summarizes the developing therapies that target the inflammasome unit. This review has taken up one of the foremost endeavours in understanding and inhibiting the NLRP3 inflammasome as a means of generating safer pharmacological therapies.
药物诱导的毒性是临床医学中的一个重要问题,通常会导致器官功能障碍和不良健康后果。NOD样受体(NLR)家族包括参与识别病原体和触发先天免疫反应的细胞内蛋白,包括NLRP3炎性小体的激活。NLRP3(含核苷酸结合寡聚化结构域样受体家族,含pyrin结构域3)炎性小体是先天免疫和适应性免疫反应的关键组成部分,并且与各种药物诱导的毒性有关,包括肝脏、肾脏和心血管疾病。NLRP3炎性小体的异常激活会导致促炎细胞因子如IL-1β和IL-18的释放,这会导致对组织的更多损伤。靶向NLRP3炎性小体是抑制药物诱导毒性的一种潜在治疗手段。本综述深入探讨了NLRP3炎性小体的机制、药物诱导的器官毒性、治疗策略和前瞻性治疗方法,并总结了针对炎性小体单元的正在开发的疗法。本综述是在理解和抑制NLRP3炎性小体作为产生更安全药物疗法手段方面所做的最重要努力之一。