miR-548j-5p Regulates Angiogenesis in Peripheral Artery Disease

The effects of specific miRNAs on angiogenesis were evaluated by assessing the in vitro angiogenic function of endothelial progenitor cells, performing an in vivo angiogenesis assay, and employing a mouse hindlimb ischemic model.
[Scientific Reports]
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Pre-Configuring Chromatin Architecture with Histone Modifications Guides Hematopoietic Stem Cell Formation in Mouse Embryos

The authors performed multi-omics dissection of the hematopoietic stem cell (HSC) ontogeny trajectory across early arterial endothelial cells (ECs), hemogenic ECs, pre-HSCs and long-term HSCs in mouse embryos.
[Nature Communications]
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MEG8 Regulates Tissue Factor Pathway Inhibitor 2 (TFPI2) Expression in the Endothelium

Scientists investigated the role of maternally expressed gene 8 (MEG8) specifically in endothelial function as well as the underlying mechanism, hypothesizing that it plays an important role in cardiovascular disease via epigenetic regulation of gene expression.
[Scientific Reports]
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Liraglutide Prevents High Glucose Induced HUVECs Dysfunction via Inhibition of PINK1/Parkin-Dependent Mitophagy

Investigators characterized the potential effects of liraglutide, a glucagon-like peptide-1 receptor agonist, on preventing high glucose-induced endothelial dysfunction and excessive mitophagic response.
[Molecular and Cellular Endocrinology]
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Tumors Resurrect an Embryonic Vascular Program to Escape Immunity

It is assumed that angiogenesis-induced suppression of adhesion molecules is a regulatory function to provide an embryo with immune privileged conditions and allow uninterrupted growth and development. It is becoming clear that similar conditions are used by tumors to evade the immune system and ensure progressive growth.
[Science Immunology]
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Cardiovascular Ramifications of Therapy-Induced Endothelial Cell Senescence in Cancer Survivors

The authors discuss the mechanisms of cancer therapy-induced senescence, focusing on endothelial cell senescence since it has been shown to be a key player in numerous cardiovascular complications.
[Biochimica Et Biophysica Acta-Molecular Basis of Disease]
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Exact Sciences and OncXerna Announce Licensing Agreement to Help Predict Immunotherapy Response for More Patients

Exact Sciences Corp. and OncXerna Therapeutics, Inc. announced they have entered an exclusive license agreement to bring OncXerna’s Xerna tumor microenvironment (TME) Panel lab services to more US patients. The Xerna TME Panel is an innovative gene expression score that helps identify patients likely to respond to anti-angiogenic and immunotherapies.
[Exact Sciences Corporation]
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REGENXBIO Announces Initiation of Second Pivotal Trial in RGX-314 Clinical Program for the Treatment of Wet AMD Using Subretinal Delivery

REGENXBIO, Inc. announced the initiation of ASCENTTM, the second of two Phase III pivotal trials to evaluate the efficacy and safety of subretinal delivery of RGX-314 in patients with wet age-related macular degeneration (wet AMD).
[REGENXBIO, Inc.]
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Endothelial-Derived Extracellular microRNA-92a Promotes Arterial Stiffness by Regulating Phenotype Changes of Vascular Smooth Muscle Cells

The authors investigated the role of endothelial-derived extracellular microRNA-92a in promoting arterial stiffness by regulating endothelial cell–vascular smooth muscle cell communication.
[Scientific Reports]
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Engineered Human Blood–Brain Barrier Microfluidic Model for Vascular Permeability Analysis

The authors described an in vitro model of the human blood–brain barrier self-assembled within microfluidic devices from stem-cell-derived or primary brain endothelial cells, and primary brain pericytes and astrocytes.
[Nature Protocols]
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CU06-1004 Enhances Vascular Integrity and Improves Cardiac Remodeling by Suppressing Edema and Inflammation in Myocardial Ischemia–Reperfusion Injury

Investigators found that CU06-1004, as a vascular leakage blocker, could improve cardiac function by inhibiting cardiac microvascular endothelial cells’ hyperpermeability and subsequently reducing the neutrophil’s plugging and infiltration in infarcted hearts.
[Experimental and Molecular Medicine]
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