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This editorial refers to ‘Arterial injury promotes medial chondrogenesis in Sm22 knockout mice’ by J. Shen et al ., pp. 28–37, this issue. Vascular medial calcification (VMC), also known as Monckeberg's medial sclerosis, is commonly associated with ageing and occurs in patients with type II diabetes mellitus (T2D) and end-stage renal disease (ESRD). In these cases, calcium phosphate salts deposit in arterial mediae associated with elastin/collagen-rich extracellular matrix, typically in a linear fashion along the elastic lamina of arterial mediae. As the lesion advances, the mediae are filled with circumferential rings of calcium phosphate crystals, resulting in decreased vessel wall compliance that leads to increased arterial pulse wave velocity and pressure, impaired coronary artery perfusion, and cardiovascular dysfunction.1 In T2D and ESRD patients, arterial medial calcification is highly prevalent and believed to be a major risk factor for cardiovascular mortality, stroke, and lower-limb amputation.2–4VMC has long been considered a degenerative process leading to passive deposition of calcium phosphate salts associated with tissue necrosis. However, the presence of bone- and cartilage-related proteins, osteoblast- and chondrocyte-like cells, and outright bone- and cartilage-like tissue in calcified lesions has underscored its cell-mediated, actively regulated nature that resembles, at least in part, embryonic bone formation and remodelling.2,5–7 …

Smooth muscle cells in pathogenesis of vascular medial cartilaginous metaplasia