Human Valvular Interstitial Cells (hVICs) are primary fibroblast-like cells isolated from normal human aortic valve tissue. These cells exhibit fibroblast-like morphology with elongated, spindle-shaped profiles under standard culture conditions. Functionally, hVICs participate in valvular homeostasis, but under pathological stimuli, they contribute to calcific aortic valve disease (CAVD) through osteogenic differentiation, a process marked by upregulated alkaline phosphatase (ALP) and collagen type I expression (1). Inflammatory pathways such as NLRP3 inflammasome activation and TGF-β signaling, further exacerbate extracellular matrix (ECM) stiffening and calcium deposition, both hallmarks of CAVD progression (2). Immunophenotyping confirms their identity through positive staining for vimentin and α-SMA, while remaining negative for endothelial markers such as Factor VIII. hVICs require careful handling, repeated freeze-thaw cycles should be avoided to maintain optimal viability.
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