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The mechanism underlying Shprintzen–Goldberg syndrome is solved and reveals that missense mutations in the transcriptional repressor SKI abolish ligand-induced SKI degradation, which results in attenuation of TGF-β transcriptional responses.

Flow-dependent remodeling of blood vessels is critical for normal physiology and for recovery from arterial blockage in disease; understanding its cellular mechanisms may lead to the development of treatments for patients that are deficient in this process following myocardial infarction or other vascular diseases.

The m1A modification plays vital roles in the regulation of the biological functions of multiple RNA species (including mRNA, lncRNA, and circRNA) and influences the interactions between these RNAs.

Transcriptome analysis reveals an alternative splicing program induced in the arterial endothelium under low-flow inflammatory conditions by platelet and macrophage recruitment and dependent upon the RNA-binding splice factor Rbfox2.

Genetic analyses reveal the importance of dynamic protein processing at the apical cell membrane in response to forces damaging cell membranes during tube expansion in tubular organs.

A GWAS meta-analysis for OPLL identified fourteen significant genomic loci and a subsequent Mendelian randomization study provided genetic evidence for a causal effect of obesity on the pathogenesis of OPLL, especially one of its subtypes, thoracic OPLL.

Alk5/TGF-β signaling is required in the endothelium to orchestrate zebrafish cardiac outflow tract morphogenesis, regulating smooth muscle cell and extracellular matrix organization.

Calcium channel blockers accelerate aortic aneurysm and cause premature aortic rupture in a mouse model of Marfan syndrome through protein kinase C-mediated activation of extracellular signal-regulated kinase.

Persistent Coxiella burnetii infected abdominal aorta aneurysms are associated with an immune-suppressed microenvironment.