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This mechanism not only ensures targeted drug delivery but also allows for diffusion to adjacent non-targeted cells, resulting in potential bystander effects that enhance therapeutic efficacy [3]

These effects were linked to GAs capacity to suppress levels of PPAR-, elevate concentrations of NO, H2O2, and malondialdehyde, and activate the Ras/Raf/JAK/STAT signaling pathways

GlycoATP and mitoATP were derived from cells sequentially treated with oligomycin A and Rot/Antimycin A

Chondrocytes respond to G6PDH deletion by reducing protein load through UPR activation and by increasing protein degradation to minimize ER stress-induced chondrocyte cell death (Fig

Tolerability (preclinical): Each peptide is generally well tolerated in animal studies, with occasional mild injection-site reactions