Microcystin-LR Drives Early NAFLD Pathogenesis via Hepatic Cholesterol Accumulation: Dysregulation of <i>Ldlr</i> and <i>Abcg1</i> Expression Uncoupled from <i>Srebp2</i>.

Although this difference reached borderline significance in the univariate analysis ( p = 0.05), its relevance to the overall toxicological profile was robustly substantiated by subsequent multivariate analyses (see Section 2.5 ), where it was identified as a key driver of the toxicity model.

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As shown in Figure 4 A, Cyp3a2 mRNA levels exhibited an increasing trend in the microcystin-LR group compared to the control.

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Although the mean mRNA expression of Pcsk9 —which promotes LDLR degradation—appeared lower in the microcystin-LR group (consistent with reduced SREBP-2 activity), this difference did not reach statistical significance ( Figure 2 C).

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However, the validity of our conclusion regarding the functional upregulation of LDLR is robustly supported by the triangulation of three independent lines of evidence: “Phenotypic Anchoring,” “Mechanistic Congruence,” and “Statistical Bridging.” Phenotypic Anchoring (Deductive Logic): We observed a highly significant accumulation of hepatic total cholesterol ( Table 2 ) as a functional endpoint.

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