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Arner EN, Rathmell JC

Chronic inflammation is sustained by the constitutive activation of key signaling pathways such as NF-B, JAK/STAT, p38 MAPK, COX-2, ERK, mTOR, and AP-1, which drive transcription of genes involved in inflammation, survival, and proliferation [39]

Restoring its function via Caveolin-1 overexpression has been shown to inhibit ferroptosis by improving mitochondrial homeostasis, thereby mitigating cognitive decline both in vitro and in vivo (67)

However, when you have too many unstable molecules floating around (and not enough antioxidants), it can lead to cellular damage, illness, and aging and sets the stage for chronic and degenerative diseases