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The PTHrP/PPAR signaling pathway has been reported to participate in nicotine-induced pulmonary dysplasia in offspring

Because SELENOF has a thioredoxin-like catalytic site, SELENOF is thought to either regulate UGGT activity or the redox state of UGGT substrates (32)

Accessed July 19, 2022

Clin Exp Immunol , 1986

[43] revealed that initially, the increased hepatic lipid availability in obese individuals with NAFLD enhances hepatic mitochondrial competence, however, it eventually stimulates enhanced hepatic oxidative stress and therefore, decreases mitochondrial activity, promoting the development of NAFLD into NASH [44]