Fig. 8: Graphical model of vessel size control during vascular remodelling. | Nature Communications

Fig. 8: Graphical model of vessel size control during vascular remodelling.

From: Circumferential actomyosin bundles anchored by CCM1 drive endothelial cell contraction and vessel constriction

Fig. 8: Graphical model of vessel size control during vascular remodelling.

Between 2 and 4 dpf, zebrafish ISVs elongate while simultaneously undergoing radial constriction, even as EC numbers increase through division and cell exchange. This paradox is resolved by circumferential actin bundles, anchored by Krit1/CCM1 at cell-cell junctions and reinforced by myosin II, which generate contractile forces that drive EC contraction and rearrangement. These coordinated cytoskeletal mechanisms allow vessels to narrow while accommodating additional cells. When actomyosin activity or Krit1 function is disrupted, ECs fail to contract and rearrange, resulting in vessel dilation. This model highlights how EC mechanics, through the integration of actin, myosin II and Krit1, regulate vessel diameter during vascular remodelling.

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