Skip to main content
. Author manuscript; available in PMC: 2016 Dec 1.
Published in final edited form as: J Cardiovasc Transl Res. 2016 Feb 29;9(2):135–144. doi: 10.1007/s12265-016-9683-3

Fig. 6.

Fig. 6

The proposed novel mechanism of caspase-1 in development of CKD-promoted NH. 1 The NLR/inflammasome caspase-1 pathway in the contractile VSMCs senses the uremic toxins as DAMPs in a CKD-state, which consequently activates caspase-1. The activation of caspase-1 promotes the maturation and secretion of pro-inflammatory cytokines IL-1b and IL-18, decreases the expression of VSMC contractile markers and presumably makes VSMCs switch to synthetic phenotype and induce proliferation. 2 Caspase-1 activation in the contractile weakened VSMCs increases the expression of integrin αvβ3, which mediates the formation of NH induced by inward remodeling due to the migration of VSMCs, leading to stenotic arterial lesion, occlusion of arterial lumen, and causes obstruction to the blood flow