Conclusions: The data suggest that hypertrophic cardiomyocytes secrete elevated levels of KMV, which paracrinally increases nuclear accumulation of Meox2 in ECs, where Meox2 binds to the promoter of p21 and thereby triggers EC senescence and subsequent angiogenesis impairment, ultimately driving capillary rarefaction to promote PO-induced HF. The gene discussed is MEOX2; the disease is hydrops fetalis.