Chemotherapy-induced peripheral neuropathy (CIPN) is a debilitating side effect with limited treatment options. The primary challenge in developing therapies is the lack of identified neurotoxic mechanisms. To address this, an integrated omics approach, combining transcriptomics, proteomics, and metabolomics, is essential to map the biological changes underlying the condition. Here, we show how data from these complementary approaches converge on key mechanisms involved in CIPN through a critical summary of animal and human studies. Current research highlights several key drivers of CIPN, such as inflammatory signaling and oxidative stress, mitochondrial dysfunction, and disrupted lipid metabolism. Although most data currently stem from preclinical models, the pathways identified offer promising targets for biomarker discovery and treatment. To translate these findings into clinical applications, integrated omics studies in human samples are urgently needed, focusing on a personalized approach. Future breakthroughs depend on large-scale human studies to tailor antineoplastic choices and neuroprotective treatments to individual patient needs.
Piga et al. (2026) studied this question.