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However, accumulating evidence over recent years has revealed that the onset and progression of OA are also profoundly influenced by immune-inflammatory responses, metabolic reprogramming, oxidative stress, and multiple forms of programmed cell death (4)

Conversely, nicotine may exert paradoxical inhibitory effects by activating immune pathways and inducing apoptosis, such as through stimulation of immature dendritic cells via PI3K/Akt signaling and modulation of caspase-3 and Cyclin B1 expression through 7-nAChR signaling [36]

Vincent, P

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