Chemotherapy-Induced Mucositis: A Comprehensive Review of ROS, Inflammasome Activation, and Therapeutic Interventions
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Chemotherapy-induced mucositis (CIM) is a significant and often severe complication of cancer treatment, characterized by inflammation and ulceration of the mucosal lining throughout the gastrointestinal tract. This debilitating condition not only severely impacts patient quality of life by causing pain, difficulty eating, and increased risk of infection, but also frequently necessitates dose reductions or treatment interruptions, ultimately affecting overall treatment outcomes. This review summarizes the pathophysiological mechanisms underlying CIM, emphasizing the essential roles of reactive oxygen species(ROS), inflammation, inflammasome activation, and cellular organelle dysfunction. The main molecular mediators involved, such as ROS, proinflammatory cytokines, and NLRP3 inflammasome, and potential therapeutic interventions targeting these pathways are discussed. We will carefully review the successive phases in the evolution of mucositis, from epithelial insult to progression and ulceration to healing. This review discusses the primary molecular mediators involved: ROS, proinflammatory cytokines, transcription factor NF-κB, NLRP3 inflammasome, mitochondria, and endoplasmic reticulum (ER) stress. We also explore the therapeutic landscape and discuss potential interventions against these key pathways, followed by discussing future steps to improve CIM management. This review aims to comprehensively analyze the therapeutic landscape and propose targeted interventions against key pathways involved in CIM, ultimately outlining future strategies to significantly improve CIM management.
Abstract
Chemotherapy-induced mucositis (CIM) is a significant and often severe complication of cancer treatment, characterized by inflammation and ulceration of the mucosal lining throughout the gastrointestinal tract. This debilitating condition not only severely impacts patient quality of life by causing pain, difficulty eating, and increased risk of infection, but also frequently necessitates dose reductions or treatment interruptions, ultimately affecting overall treatment outcomes. This review summarizes the pathophysiological mechanisms underlying CIM, emphasizing the essential roles of reactive oxygen species(ROS), inflammation, inflammasome activation, and cellular organelle dysfunction. The main molecular mediators involved, such as ROS, proinflammatory cytokines, and NLRP3 inflammasome, and potential therapeutic interventions targeting these pathways are discussed. We will carefully review the successive phases in the evolution of mucositis, from epithelial insult to progression and ulceration to healing. This review discusses the primary molecular mediators involved: ROS, proinflammatory cytokines, transcription factor NF-κB, NLRP3 inflammasome, mitochondria, and endoplasmic reticulum (ER) stress. We also explore the therapeutic landscape and discuss potential interventions against these key pathways, followed by discussing future steps to improve CIM management. This review aims to comprehensively analyze the therapeutic landscape and propose targeted interventions against key pathways involved in CIM, ultimately outlining future strategies to significantly improve CIM management.