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Expression of the CD30 ligand (CD30L) on human peripheral blood lymphocytes from normal donors and patients with lymphoid malignancies
These lignans, including schisandrin B (Sch B), schisandrin A (Sch A), and deoxyschisandrin (DS), have been demonstrated to ameliorate MASLD through multiple mechanisms: activation of PPAR- to promote fatty acid (FA) oxidation, inhibition of the LXR-/sterol regulatory element-binding protein 1c (SREBP-1c)/FAS pathway to reduce de novo lipogenesis, activation of the AMPK/mTOR autophagy pathway to decrease hepatic lipid accumulation, and suppression of pro-inflammatory cytokines to attenuate hepatic inflammation
In view of this continuity, the following discussion traces these events as a mechanistic cascade, starting with defective ERmitochondria calcium coupling, continuing through redox injury and impaired mitochondrialysosome quality control, and then considering interfaces that govern polarity, metabolism, transcriptional adaptation, and inflammatory amplification
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