Deficiency Promotes Pulmonary Arterial Hypertension via HGF/c-Met Signaling.

Background: In large-scale genomic studies, , an endothelial-specific transcription factor, has been suggested as a putative causal gene of pulmonary arterial hypertension (PAH); however, its role and molecular mechanisms remain to be elucidated. We investigated the functional impacts and acting mechanisms of impaired Sox17 (SRY-related HMG-box17) pathway in PAH and explored its potential as a therapeutic target.

Methods: In adult mice, deletion in pulmonary endothelial cells (ECs) induced PAH under hypoxia with high penetrance and severity, but not under normoxia.

Left Ventricular Ejection Fraction 1 Year After Acute Myocardial Infarction Identifies the Benefits of the Long-Term Use of β-Blockers: Analysis of Data From the KAMIR-NIH Registry.

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Hypertension Burden and the Risk of New-Onset Atrial Fibrillation: A Nationwide Population-Based Study.

The association between the cumulative hypertension burden and the development of atrial fibrillation (AF) is unclear. We aimed to investigate the relationship between hypertension burden and the development of incident AF. Using the Korean National Health Insurance Service database, we identified 3 726 172 subjects who underwent 4 consecutive annual health checkups between 2009 and 2013, with no history of AF.

Dll4 Suppresses Transcytosis for Arterial Blood-Retinal Barrier Homeostasis.

Rationale: Central nervous system has low vascular permeability by organizing tight junction (TJ) and limiting endothelial transcytosis. While TJ has long been considered to be responsible for vascular barrier in central nervous system, suppressed transcytosis in endothelial cells is now emerging as a complementary mechanism. Whether transcytosis regulation is independent of TJ and its dysregulation dominantly causes diseases associated with edema remain elusive.