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Aug 30 1994;112(24):328-330

This is where the story gets specific

A major role for ferroptosis in Mycobacterium tuberculosisinduced cell death and tissue necrosis

In conditions of low body iron, Fe 2+ is mobilized into circulation through two pathways: either directly exported through ferroportin-1 (FPN1) on the basal membrane, where it is oxidized to Fe 3+ by copper-containing iron oxidases, such as ceruloplasmin and hephaestin, or by FTN degradation via autophagy mediated by nuclear receptor coactivator 4 (NCOA4)

BPC-157 relies on adequate blood flow to reach target tissues, and even mild dehydration can impair circulation and slow nutrient delivery to healing sites

Granulosa cells of developing follicles express VDR and the enzymes for local calcitriol synthesis, creating an autocrine/paracrine loop (94)
