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Exp Mol Med 2022 Aug 5. Epub 2022 Aug 5.

Gene and Cell Therapy Research Center for Vessel-Associated Disease, Medical Research Institute, and Department of Pharmacology, Pusan National University School of Medicine, Yangsan, 50612, Republic of Korea.

Retinal angiogenesis was delayed in VSMC-specific Akt1-deficient mice (Akt1) but not in Akt2 mice. The proliferation of ECs, recruitment of pericytes, and coverage of VSMCs to the endothelium were defective in Akt1. The silencing of Akt1 in VSMCs led to the downregulation of angiopoietin 1 (Ang1) and the upregulation of Ang2. Read More

Front Cardiovasc Med 2022 22;9:911649. Epub 2022 Jun 22.

Center for Pulmonary Arterial Hypertension and Pulmonary Vascular Disease, China Medical University Hospital, Taichung, Taiwan.

Background: Genetic variants could be identified in subjects with idiopathic and heritable pulmonary arterial hypertension (PAH). The 6th World Symposium on Pulmonary Hypertension (WSPH) provided a list of genes with evidence of association with PAH. However, reports using whole exome sequencing (WES) from southeastern Asian PAH cohorts were scarce. Read More

Vascul Pharmacol 2022 Jul 2;145:107087. Epub 2022 Jul 2.

Center for Cardiovascular Research and The Heart Center, Nationwide Children's Hospital, The Ohio State University, Columbus, OH, USA; Department of Pediatrics, The Ohio State University, Columbus, OH, USA. Electronic address:

Background: Notch signaling is an evolutionarily conserved pathway that functions via direct cell-cell contact. The Notch ligand Jagged1 (Jag1) has been extensively studied in vascular development, particularly for its role in smooth muscle cell maturation. Endothelial cell-expressed Jag1 is essential for blood vessel formation by signaling to nascent vascular smooth muscle cells and promoting their differentiation. Read More

Cureus 2022 Jul 1;14(7):e26495. Epub 2022 Jul 1.

Internal Medicine, Hospital da Senhora da Oliveira, Guimarães, PRT.

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is the most common and best-known monogenic small vessel disease. This disease is caused by a genetic mutation in the neurogenic locus notch homolog protein 3 (NOTCH3) gene, inherited as an autosomal dominant trait, the presence of which confirms the diagnosis of CADASIL. Clinically, it can express itself in a variety of symptoms, including migraine with aura, mood disturbance, vascular dementia, ischemic stroke, and premature death. Read More

Front Neurol 2022 14;13:881528. Epub 2022 Jun 14.

Department of Neurology, Kumamoto University, Kumamoto, Japan.

This study aimed to evaluate the utility of immunohistochemical staining of vascular Notch3 deposits in biopsied unfixed frozen skin samples from patients with suspected cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL). We analyzed vascular Notch3 deposits in unfixed frozen skin biopsy samples obtained from 43 patients with suspected CADASIL by immunohistochemistry using antibodies against the extracellular domain (ECD) of Notch3. We also sequenced the gene in all patients, as well as evaluated their symptoms and neuroimages. Read More