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In addition, the reactive oxygen species produced in response to nicotine also induces mesangial cell proliferation and extracellular matrix deposition through pathways that involve increased expression of cyclooxygenase 2-derived prostaglandins and increased phosphorylation of extracellular signal-regulated protein kinases 1 and 2, c-Jun N-terminal kinases, activator protein 1, and protein kinase B

The persistent limitation is translational: rodent lipid handling differs from human physiology, and even the best diet models only partially recapitulate the slow, heterogeneous fibrotic progression seen in human MASH which is why an animal liver-fat signal is treated as hypothesis-generating rather than confirmatory

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Several key trends characterize the current landscape

Newell 2012