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3.2.1 Lactate accumulation and targeting LDHA in pulmonary fibrosis Emerging studies indicate that metabolic reprogramming in AEC2 contributes to lactate accumulation in pulmonary fibrosis, which exacerbates fibrotic progression by activating TGF-/mTOR signaling and suppressing anti-fibrotic miRNAs such as the miR200 family (Song et al., 2022
Bioinformatics 26 , 139140 (2009)
Extended-release oxybutynin therapy for vasomotor symptoms in women: a randomized clinical trial
Cancers 12 , 2195 (2020)
In the future, larger amounts of clinical data will be needed to draw more comprehensive and rational conclusions
