• EGCG dose-dependently reduces calcium phosphate deposition and osteogenic differentiation of vascular smooth muscle cells (VSMCs) in vivo and in vitro.
• JunB is identified as a key transcription factor activated in CKD-associated medial arterial calcification and osteoblast-like VSMCs.
• EGCG suppresses vascular calcification by inhibiting JunB activity, with JunB overexpression abolishing and knockdown enhancing its inhibitory effect.
• The therapeutic effect of EGCG is mediated via modulation of the JunB-dependent Ras/Raf/MEK/ERK signaling pathway, offering a potential treatment for CKD-associated MAC.