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Reprogramming of Vascular Smooth Muscle Cells into Calcifying Cells: What Can We Learn from the Embryo?
Author(s) -
Kempf Hervé
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.190.3
Subject(s) - vascular smooth muscle , mural cell , calcification , biology , reprogramming , embryonic stem cell , microbiology and biotechnology , cartilage , anatomy , pathology , smooth muscle , medicine , endocrinology , cell , gene , biochemistry , genetics
Vascular calcifications are widespread in aged individuals and patients with atherosclerosis, diabetes or chronic renal failure. These calcifications of the blood vessels are mostly due to a phenotypic switch of vascular smooth muscle cells (VSMCs) that reprogram into calcifying cells through mechanisms and gene regulations that mimic embryonic bone formation. Over the years, a regiment of systemic factors has been shown to induce VSMCs to trans‐differentiate into cartilage or bone cells and eventually calcify. However, in vivo, vascular calcifications do not form in a randomized pattern, suggesting that intrinsic properties of VSMCs happen to play a role in the occurrence of the calcified lesions. As VSMCs derive from various independent origins during development, evidence will be put forward to prove that VSMCs are differentially prone to calcify within the vascular wall upon their heterogeneous embryological origin.