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Role of the Lymphatics in Cardiac Disease
Arterioscler Thromb Vasc Biol. 2024 Apr 18. doi: 10.1161/ATVBAHA.124.319854. Online ahead of print.ABSTRACTCardiovascular diseases remain the largest cause of death worldwide with recent evidence increasingly attributing the development and progression of these diseases to an exacerbated inflammatory response. As a result, significant research is now focused on modifying the immune environment to prevent the disease progression. This in turn has highlighted the lymphatic system in the pathophysiology of cardiovascular diseases owing, in part, to its established function in immune cell surveillance and trafficking. In this ...
Source: Arteriosclerosis, Thrombosis and Vascular Biology - April 18, 2024 Category: Cardiology Authors: Susanna T E Cooper Adam B Lokman Paul R Riley Source Type: research

Atherosclerotic Plaque Epigenetic Age Acceleration Predicts a Poor Prognosis and Is Associated With Endothelial-to-Mesenchymal Transition in Humans
CONCLUSIONS: Plaque EAA is a strong and independent marker of poor outcome in patients with severe atherosclerosis. Plaque EAA was linked to mesenchymal endothelial and smooth muscle cells. Endothelial-to-mesenchymal transition was associated with EAA, which was experimentally validated. Epigenetic aging mechanisms may provide new targets for treatments that reduce atherosclerosis complications.PMID:38634280 | DOI:10.1161/ATVBAHA.123.320692 (Source: Arteriosclerosis, Thrombosis and Vascular Biology)
Source: Arteriosclerosis, Thrombosis and Vascular Biology - April 18, 2024 Category: Cardiology Authors: Ernest Diez Benavente Robin J G Hartman Tim R Sakkers Marian Wesseling Yannicke Sloots Lotte Slenders Arjan Boltjes Barend M Mol Gert J de Borst Dominique P V de Kleijn Koen H M Prange Menno P J de Winther Johan Kuiper Mete Civelek Sander W van der Laan S Source Type: research

Resident Memory T Cells in the Atherosclerotic Lesion Associate With Reduced Macrophage Content and Increased Lesion Stability
CONCLUSIONS: TRM cells, characterized by the expression of CD69 and CD49α, constitute a minor population in atherosclerotic lesions and are associated with increased lesion stability in a Hobit and Blimp-1 knockout mouse model.PMID:38634281 | DOI:10.1161/ATVBAHA.123.320511 (Source: Arteriosclerosis, Thrombosis and Vascular Biology)
Source: Arteriosclerosis, Thrombosis and Vascular Biology - April 18, 2024 Category: Cardiology Authors: M J M de Jong M A C Depuydt F H Schaftenaar K Liu D Maters Anouk Wezel Harm J Smeets J Kuiper I Bot K van Gisbergen B Sl ütter Source Type: research

Arterial Smooth Muscle Cell AKAP150 Mediates Exercise-Induced Repression of Ca < sub > V < /sub > 1.2 Channel Function in Cerebral Arteries of Hypertensive Rats
CONCLUSIONS: The current study demonstrates that aerobic exercise ameliorates CaV1.2 channel function via inhibiting myocyte AKAP150, which contributes to reduced cerebral arterial tone in hypertension.PMID:38602101 | DOI:10.1161/ATVBAHA.124.319543 (Source: Arteriosclerosis, Thrombosis and Vascular Biology)
Source: Arteriosclerosis, Thrombosis and Vascular Biology - April 11, 2024 Category: Cardiology Authors: Yanyan Zhang Zhaoxia Xu Meiling Shan Jiaqi Cao Yang Zhou Yu Chen Lijun Shi Source Type: research

Endothelial Cell Flow-Mediated Quiescence Is Temporally Regulated and Utilizes the Cell Cycle Inhibitor p27
CONCLUSIONS: Endothelial cell flow-mediated quiescence has unique properties and temporal regulation of quiescence depth that depends on the flow stimulus. These findings are consistent with a model whereby flow-mediated endothelial cell quiescence depth is temporally regulated downstream of p27 transcriptional regulation by HES1 and ID3. The findings are important in understanding endothelial cell quiescence misregulation that leads to vascular dysfunction and disease.PMID:38602102 | DOI:10.1161/ATVBAHA.124.320671 (Source: Arteriosclerosis, Thrombosis and Vascular Biology)
Source: Arteriosclerosis, Thrombosis and Vascular Biology - April 11, 2024 Category: Cardiology Authors: Natalie T Tanke Ziqing Liu Michaelanthony T Gore Pauline Bougaran Mary B Linares Allison Marvin Arya Sharma Morgan Oatley Tianji Yu Kaitlyn Quigley Sarah Vest Jeanette Gowen Cook Victoria L Bautch Source Type: research

Coronary Artery Disease Risk Variant Dampens the Expression of CALCRL by Reducing HSF Binding to Shear Stress Responsive Enhancer in Endothelial Cells In Vitro
CONCLUSIONS: Overall, our results demonstrate the existence of an endothelial-specific HSF (heat shock factor)-regulated transcriptional enhancer that mediates CALCRL expression. A better understanding of CALCRL gene regulation and the role of single-nucleotide polymorphisms in the modulation of CALCRL expression could provide important steps toward understanding the genetic regulation of shear stress signaling responses.PMID:38602103 | DOI:10.1161/ATVBAHA.123.318964 (Source: Arteriosclerosis, Thrombosis and Vascular Biology)
Source: Arteriosclerosis, Thrombosis and Vascular Biology - April 11, 2024 Category: Cardiology Authors: Ilakya Selvarajan Miika Kiema Ru-Ting Huang Jin Li Jiayu Zhu Petri P ölönen Tiit Örd Kadri Õunap Mehvash Godiwala Anna Kathryn Golebiewski Aarthi Ravindran Kiira M äklin Anu Toropainen Lindsey K Stolze Maximiliano Arce Peetra U Magnusson Stephen Whit Source Type: research