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[40] demonstrated in vitro that a decrease in endogenous N/OFQ, or the absence of its receptor, results in an increase in capsaicin-induced bronchoconstriction, indicating the ability of this neuropeptide to modulate bronchoconstriction by affecting sensory fibers

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Cell death in these experiments was suppressed by co-treatment with the specific ferroptosis inhibitor ferrostatin-1, confirming that p53 stabilization did not alter the mode of cell death induced by erastin2 (Fig 1C)

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