This study mainly illustrated that: (a) high levels of PTH contributed to VC in CKD rats; (b) PTH mediated valvular EndMT by reducing miR‐29a‐5p; (c) AAV‐miR‐29a inhibited EndMT by inhibiting the activity of γ‐secretase by targeting GSAP to block the activation of the Notch1 pathway; (d) inhibition of the Notch1 pathway blocked VC in CKD rats. The gene discussed is PTH; the disease is chronic kidney disease.