A high-phosphorus diet induced severe vascular calcification, decrease of renal function and higher mortality in uremic rats.
Proteomics showed a distinct protein expression between non-calcified and calcified aortas, with lamin increase in the latter.
VSMCs in calcifying media showed an increased binding of lamin with RUNX2, a major pro-osteoblastic transcription factor.
Successful silencing of lamin prevented VSMCs' calcification and impaired the nuclear localization of RUNX2.
Lamin A could play a key role in vascular calcification partly facilitating the nuclear localization of RUNX2.