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Crucial information about the several neurotoxicity mechanisms suggested in the literature and effective triggering events is either missing or controversial, due to heterogeneity of experimental models used to investigate such processes. To fill this knowledge gap, we compared the neurotoxicity of bortezomib (BTZ) and carfilzomib (CFZ), a less neurotoxic drug, by investigating preclinical models and dissecting the underlying molecular mechanisms using a multidimensional approach.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Experimental Approach<\/jats:title>\n                    <jats:p>We developed a new mouse model of CFZ\u2010induced neuropathy and compared it with an established BTZ model using behavioural, morphological\/morphometric and proteomic analyses of dorsal root ganglia (DRG) tissues. Mitotoxicity and cytoskeleton alterations were compared in terms of onset of altered mitochondrial morphology, functionality and trafficking, alongside cytoskeletal protein expression and axonal degeneration in cultured mouse DRG neurons.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Key Results<\/jats:title>\n                    <jats:p>BTZ's severe neurotoxicity in vivo correlated with severe loss of nerve fibres and extensive protein expression changes. In vitro, both compounds significantly altered mitochondrial network organization and energy production after 24\u2009h of treatment. However, only BTZ induced accumulation of tubulin post\u2010translational modifications and early axonal degeneration within the first 10\u00a0h, severely impacting mitochondrial trafficking after 24\u2009h.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions and Implications<\/jats:title>\n                    <jats:p>These results point to mitochondrial toxicity as a common downstream effect of both treatments, whereas BTZ\u2010specific off\u2010target activity on tubulin hyper\u2010stability may initiate early mitochondrial trafficking alterations. This knowledge may inform future mitigation approaches.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/bph.70501","type":"journal-article","created":{"date-parts":[[2026,5,28]],"date-time":"2026-05-28T12:00:15Z","timestamp":1779969615000},"page":"5120-5147","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Shared and specific molecular mechanisms of proteasome inhibitors in chemotherapy\u2010induced peripheral neurotoxicity"],"prefix":"10.1111","volume":"183","author":[{"given":"Federico","family":"Iseppon","sequence":"first","affiliation":[{"name":"Experimental Neurology Unit, School of Medicine and Surgery University of Milano\u2010Bicocca  Monza Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alessio","family":"Malacrida","sequence":"additional","affiliation":[{"name":"Experimental Neurology Unit, School of Medicine and Surgery University of Milano\u2010Bicocca  Monza 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