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Due to their large surface area, continuous exposure to environmental toxins and pathogens, and high metabolic needs related to the production of surfactants and ion transport, AECs are highly dependent on complete mitochondrial quality control mechanisms to maintain cell function and viability (Malsin and Kamp, 2018)

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In addition, accumulation of dysfunctional mitochondria due to failed mitophagy promotes a senescence-associated secretory phenotype in AECs, further amplifying pro-fibrotic signaling (Malsin and Kamp, 2018