VEGFC and cardiac hypertrophy: Persistent pressure overload reduces VEGF‐C and VEGFR‐3 expression and inactivates the downstream signals (ATK/ERK, CaNA/NFATc1/FOXC2, and CX43), which inhibits cardiac lymphangiogenesis and increases cardiac edema thereby leading to cardiac hypertrophy, fibrosis, inflammation, apoptosis, and contractile dysfunction in mice.