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The unnatural D-stereochemistry prevents recognition by most mammalian peptidases, contributing to the molecule's resistance to proteolytic degradation

Novel approaches such as organoids, vascularized tumor-on-chip models, and genetically engineered mouse models with inducible vascular and oncogenic mutations may better replicate the interplay between tumor biology and cardiovascular stress

In conclusion, we postulate that defective reticulocyte maturation is a new key pathophysiological aspect of PKD that can be classified as late stage ineffective erythropoiesis

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