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Current evidence indicates that hypoxia, oxidative stress, nutrient limitation and metabolite accumulation reprogram mitochondrial metabolism in infiltrating immune cells within the TME, whereas direct quantitative evidence for remodeling of specific mitochondrial contact sites in these cells remains limited (237)
The hypothesis has expanded to include vascular dysfunction, oxidative stress, microglial activation, and impaired proteolysis (Roda et al., 2022)
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Journal of Cellular and Molecular Medicine, 22 (11), 54395449
Multicenter, phase I, dose-escalation trial of lenalidomide plus bortezomib for relapsed and relapsed/refractory multiple myeloma
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