Research has shown that, as cysts in ADPKD expand, they exert pressure on the surrounding renal tissue and blood vessels; this compression results in localized hypoxia within the affected area, stabilizing HIF-1α in cystic epithelial cells, which then activates genes that facilitate cyst growth, including those involved in fluid secretion and cell proliferation; for instance, Kraus et al. showed that the deletion of HIF-1α in a PKD1-deficient mouse model resulted in reduced cyst growth, highlighting the role of HIF-1α in cyst progression [68]. Here, PKD1 is linked to autosomal dominant polycystic kidney disease.