The toxic side effects of chemotherapy have limited its clinical use, as chemotherapeutic agents can cause DNA damage and subsequent organ injury. The pathophysiological mechanisms of chemotherapy-induced organ injury are mediated by cascades of oxidative stress, inflammation, and apoptosis. Therefore, modulation of inflammation represents a vital role in strategies for attenuating organ injury.

Many inflammatory pathways are implicated in chemotherapy-induced organ injury, for example, nuclear factor-kappa B (NF-kB) and tumor necrosis factor-alpha (TNF-α) signaling. Activation of NF-kB signaling triggers downstream inflammatory mediators such as TNF-α, interleukin-1 (IL-1), IL-6, and IL-8, among other genes. Researchers are interested in investigating the impact of using novel agents as adjuvant therapy to alleviate the toxicity induced by chemotherapy.

The aim of this Special Issue, therefore, is to gather original research, in addition to review articles, that highlight the involvement of inflammatory cascades in the pathogenesis of organ toxicity as a result of using different kinds of chemotherapeutic agents, as well as targeting inflammation through the use of novel compounds to mitigate this injury.

Potential topics include but are not limited to the following:

• Implication of inflammatory cascades in chemotherapy-induced different organ toxicity including kidney, liver, brain, lung, and intestine
• Experimental, clinical, and in vitro studies illustrating the molecular pathophysiological mechanism of chemotherapy-induced organ injury involving inflammation
• Exploring novel inflammatory signaling implicated in chemotherapy-induced organ toxicity.
• Determination of microRNAs as well as LncRNAs linked to inflammation after chemotherapy administration
• Investigating novel agents for ameliorating organ injury induced by chemotherapeutic agents with a focus on targeting inflammatory signaling