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The core mechanism by which cells sense and respond to hypoxia relies on HIFs

1,2 In contrast, the cell death mechanisms of intrinsic hepatotoxins, particularly acetaminophen (APAP), have been extensively investigated due to their clinical relevance

Ketogenesis occurs predominantly within the hepatic mitochondria, with carnitine palmitoyl transferase I (CPT-1) acting as the critical rate-limiting enzyme for mitochondrial fatty acid import (Figure 1)