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Importantly, neuroinflammatory processes are closely intertwined with oxidative stress and mitochondrial dysfunction, as inflammatory mediators increase reactive oxygen species production and compromise mitochondrial bioenergetics, further amplifying neuronal vulnerability (33)

Therapeutic potential of beta-arrestin-and G protein-biased agonists

Additionally, it restores mitochondrial morphology, mitochondrial energy production, and mitochondrial dynamics and inhibits oxidative stress [75]

This rearrangement was not observed when AX was incubated under the same conditions without DTT

A systematic explanation for human studies, particularly regarding the translational pathway from molecular mechanisms to clinical interventions, is still lacking