This indicates a positive effect of dietary restriction on NSC proliferation that involves BDNF levels [7]
While animal models especially mouse such as diet induced, deficiency induced, toxin induced, genetically induced or as a mixture of these modalities have provided foundational insights into the mechanisms of MASLD and MASH, the translation of these findings to human pathophysiology remains limited due to significant biological and metabolic disparities between species (295, 296)
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Only by integrating molecular, cellular, systems-level, and behavioral data, analyzed with AI and interpreted within rigorous ethical frameworks, can the field realistically design robust clinical trials and develop interventions that are both mechanistically grounded and clinically effective
