Calcific aortic valve disease: can targeting endothelial-mesenchymal transition be a new alternative to surgery?—a narrative review

CAVD progresses through complex mechanisms involving inflammation, lipid deposition, and osteoblastic differentiation. EndMT has emerged as a key driver of fibrosis and osteogenesis in valve mesenchymal cells, thereby accelerating calcification. However, its regulatory networks and pathway interactions remain incompletely understood. Further research is needed to clarify these mechanisms and develop EndMT-targeted interventions, which may offer new avenues for early diagnosis and treatment of CAVD.