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discovered that STING activation requires the cellular redox balance that GPX4 maintains, and that GPX4-deficient cells have enhanced intracellular lipid peroxidation, which leads to the carbonylation of STING at the C88 locus and the inhibition of its transport from the endoplasmic reticulum (ER) to the Golgi complex, thus specifically inhibiting the cGAS-STING pathway, and affecting the release of various immune cells (44)
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When mast cells are activated in response to progesterone, the resulting histamine surge helps explain many of the hallmark features of APD, including: Hives (urticaria) caused by histamine-induced blood vessel dilation Intense itching (pruritus) driven by histamine signaling in the skin Angioedema , or deeper swelling beneath the skin and mucous membranes Asthma-like symptoms or shortness of breath , due to histamine’s effects on airway smooth muscle This mast cell–histamine connection also clarifies why treatments that target allergic pathways are often effective in APD, even though progesterone is a hormone rather than a classic allergen
