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Overexpression of TFEB leads to degradation of bulk autophagic substrates such as damaged mitochondria (Nezich et al., 2015), long-lived protein aggregates (Martini-Stoica et al., 2016), and lipid droplets (Settembre et al., 2013), indicating the crucial role of TFEB in organelle-specific autophagy, such as mitophagy and lipophagy (Settembre et al., 2013

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This aligns with previous findings that amino acids play a pivotal role in NO regulation in mammary cells, thereby exerting antibacterial activity against LPS during inflammation (232234)

Under the stimulation of CS, macrophages, neutrophils, and lymphocytes are recruited in the small airways and the lung parenchyma to secret inflammatory factors to induce oxidative stress and pulmonary epithelial cells death [84, 85]