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This result suggests that the cnd1-K658E mutation causes segregation defects by disrupting the Cnd1-Pmc4 interaction

This is why, in combinations such as CJC + Ipamorelin, it is important to clarify whether the DAC or non-DAC version is being discussed, as these represent two fundamentally different mechanistic scenarios

A narrative structure therefore allowed us to organize the field around a mechanistic question - how mitochondria-centered contact failure reshapes acinar-cell injury - and to distinguish between well-supported findings, extrapolated mechanisms, unresolved controversies, and translational gaps