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Shear stress, hypoxia, or pharmacological stimuli, such as -adrenergic receptor stimulation, have been shown to activate signaling cascades leading to release of ATP through cystic fibrosis transmembrane conductance regulator or pannexin 1 channels (36, 53)

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This idea was supported by the fact that cells depleted of ATP via inhibition of mitochondrial respiration by antimycin A were indistinguishable from controls with respect to FA numbers and cell size (Extended Data Fig