ArticleArteriosclerosis, thrombosis, and vascular biology2025
Lats1/2 Are Essential for Developmental Vascular Remodeling and Biomechanical Adaptation to Shear Stress.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- LATS1/2 inactivation drives a distinct venous endothelial cell response that contributes to fibrotic remodeling of the lung.Science advances · 2026Article
- An Rnf213-deficient hypoperfusion model reveals Moyamoya-relevant neurovascular remodeling.Angiogenesis · 2026Article
- Hemodynamics in heart: the critical role of hemodynamics in myocardial tissue development and regenerative remodeling.International journal of cardiology. Heart & vasculature · 2026Review
- Pulsatile flow dynamics maintain pulmonary artery architecture.JCI insight · 2026Article
- Mechanobiology of the Hippo-YAP Signaling Network.Cold Spring Harbor perspectives in biology · 2026Article
- Cell type specificity of Hippo-YAP signaling in cardiac development and disease.Journal of molecular and cellular cardiology · 2025Review
- Hippo in smooth muscle - a therapeutic target in vascular diseases driven by aging and hypertension.Frontiers in physiology · 2025Review
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
backgroundMechanical cues exerted by shear stress from blood flow remodel an initial vascular plexus into a ramifying array of large and small vessels. Hemodynamic forces trigger changes in endothelial cell (EC) gene expression and dynamic alterations in cell shape and adhesion. The objective of this study is to elucidate the role of the Lats (large tumor suppressor) 1 and Lats2 (Lats1/2) Hippo pathway kinases in EC transducing of hemodynamic signals as vessels form.
methodsLats1/2 were genetically deleted in murine ECs (
resultsWe report a critical requirement for Lats1/2 in adapting to blood flow during vascular development. When Lats1/2 are genetically deleted in ECs, embryos develop severe defects in blood vessel formation, which lead to embryonic lethality by embryonic day 11.5. Vessel patterning and circulation initiate properly; however, remodeling of the initial vascular plexus fails due to lumen collapse. Lats1/2 depletion in cultured ECs leads to failed polarization, elongation, and VEcad (vascular endothelial cadherin 5 or Cdh5) junctional maturation under flow. Finally, YAP (Yes-associated protein)/TAZ (transcriptional coactivator with PDZ-binding motif) codepletion in Lats1/2 depleted conditions leads to a partial rescue of phenotypes in vivo and in vitro.
conclusionsOur results suggest that Lats1/2 deficient cells no longer respond to laminar shear stress, in vivo and in vitro. This work identifies Lats1 and Lats2 as critical transducers of biomechanical cues during early blood vessel remodeling. This study provides new targets for treating vascular diseases and new directions for efforts to generate vascularized tissues for replacement therapies.
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