Mitochondrial Dysfunction and Oxidative Stress Oxaliplatin causes morphological changes and functional deficits of mitochondria
Oxid Med Cell Longev 2014:360438 Conrad M, Pratt DA (2019) The chemical basis of ferroptosis
2012 doi: 10.1056/NEJMoa1211721
Compared to rituximab, deeper B cell depletion is being explored with antibodies targeting CD20 (obinutuzumab), CD19 (inebilizumab), CD38 (daratumumab), the BAFF receptor (ianalumab), and TACI (telitacicept), as well as proteasome inhibition with bortezomib, all showing promise in IMIDs ( A key limitation of BCDA is the increased infection risk due to prolonged B-cell depletion, concurrent immunosuppressive therapy, and hypogammaglobulinemia ( Despite a plethora of successful targeted biologic therapies with different mechanisms of action, most patients with IMID still do not achieve remission, let alone drug-free remission ( 3 From stem cell therapy to targeted cell therapy for immune mediated inflammatory diseases 3.1 Transition from stem cell therapy to chimeric antigen receptor T cell therapy In contrast to the chronic immune suppression associated with targeted biologic therapies, stem cell treatments, including both mesenchymal stem cell therapy (MSCT) and hematopoietic stem cell therapy (HSCT)present a promising approach for potentially curing IMIDs by reinducing self-tolerance
Crosstalk with mitochondria occurs at ERmitochondria contact sites (MAMs), where tightly coupled Ca and lipid exchange can propagate ROS signals bidirectionallyER stress can potentiate mitochondrial ROS production and mitochondrial dysfunction can feed back to intensify ER oxidative pressureshaping cell-wide redox tone and stress adaptation
