Bmal1 may control blood vessel hardening through an unusual body clock pathway

Bmal1 expression is selectively upregulated in diabetic arteries and vascular smooth muscle cells under hyperglycemic conditions.

• Deletion of Bmal1 in vascular smooth muscle cells significantly reduced diabetes-induced vascular calcification and aortic stiffness.
• Bmal1 is associated with increased expression of osteogenic genes in both in vivo and in vitro models of diabetes.
• RNA sequencing indicated that Bmal1 regulates genes related to bone-like differentiation and the structure of the extracellular matrix.
• Bmal1 enhances the transcription of Runx2, a key regulator of bone formation, by directly binding to its promoter region.
• The disruption of Bmal1's interaction with the Runx2 promoter resulted in the loss of Runx2 expression.

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