NLRP3 as a therapeutic target in cyclophosphamide-associated toxicities.

Cyclophosphamide (CPM), a potent chemotherapeutic agent, while effective against various cancers, can cause significant organ damage. The NLRP3 inflammasome, a key player in the innate immune response, is implicated in this toxicity. This review delves into the intricate relationship between CPM and NLRP3 inflammasome activation, focusing on oxidative stress-mediated organ damage. We explore the mechanisms by which CPM induces NLRP3 activation in the kidneys, heart, liver, and gastrointestinal tract. Additionally, we examine the signaling pathways involved in this process. The review also discusses potential therapeutic interventions, including phytotherapeutic agents, that target NLRP3 inflammasome activation to mitigate CPM-induced organ injury. By highlighting the crucial role of NLRP3 in CPM-related toxicity, this review provides a foundation for future research aimed at developing novel therapeutic strategies to minimize adverse effects and improve patient outcomes.