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

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

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

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

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

Cognitive Impairment and Brain Atrophy in Patients with Chronic Kidney Disease
In conclusion, patients with CKD are at a higher risk of developing CI, with brain atrophy being a contributing factor. Despite the identification of various preventive measures, the evidence substantiating their efficacy remains limited across all studies. Future expectations lie in large-scale randomized controlled trials.PMID:38592226 | DOI:10.3390/jcm13051401 (Source: Atherosclerosis)
Source: Atherosclerosis - April 9, 2024 Category: Cardiology Authors: Kazuhiko Tsuruya Hisako Yoshida Source Type: research

Cognitive Impairment and Brain Atrophy in Patients with Chronic Kidney Disease
In conclusion, patients with CKD are at a higher risk of developing CI, with brain atrophy being a contributing factor. Despite the identification of various preventive measures, the evidence substantiating their efficacy remains limited across all studies. Future expectations lie in large-scale randomized controlled trials.PMID:38592226 | PMC:PMC10931800 | DOI:10.3390/jcm13051401 (Source: Atherosclerosis)
Source: Atherosclerosis - April 9, 2024 Category: Cardiology Authors: Kazuhiko Tsuruya Hisako Yoshida Source Type: research

Virus-Specific T Cells in the Atheroma Crime Scene: Guilty Accomplices or Innocent Bystanders?
Arterioscler Thromb Vasc Biol. 2024 Apr 4. doi: 10.1161/ATVBAHA.124.320932. Online ahead of print.NO ABSTRACTPMID:38572645 | DOI:10.1161/ATVBAHA.124.320932 (Source: Arteriosclerosis, Thrombosis and Vascular Biology)
Source: Arteriosclerosis, Thrombosis and Vascular Biology - April 4, 2024 Category: Cardiology Authors: Anton Gister å Source Type: research

Glycoursodeoxycholic Acid Alleviates Arterial Thrombosis via Suppressing Diacylglycerol Kinases Activity in Platelet
CONCLUSIONS: Our study implicated that GUDCA reduces platelet hyperreactivity and improves thrombotic propensity by inhibiting DGKs activity, which is a potentially effective prophylactic approach and promising therapeutic agent for arterial thrombotic events.PMID:38572646 | DOI:10.1161/ATVBAHA.124.320728 (Source: Arteriosclerosis, Thrombosis and Vascular Biology)
Source: Arteriosclerosis, Thrombosis and Vascular Biology - April 4, 2024 Category: Cardiology Authors: Wenchao Yang Ruijia Feng Guiyan Peng Zhecun Wang Meifeng Cen Yexiang Jing Weiqi Feng Ting Long Yunchong Liu Zilun Li Kan Huang Guangqi Chang Source Type: research

Angiotensinogen as a Therapeutic Target for Cardiovascular and Metabolic Diseases
Arterioscler Thromb Vasc Biol. 2024 Apr 4. doi: 10.1161/ATVBAHA.124.318374. Online ahead of print.ABSTRACTAGT (angiotensinogen) is the unique precursor for the generation of all the peptides of the renin-angiotensin system, but it has received relatively scant attention compared to many other renin-angiotensin system components. Focus on AGT has increased recently, particularly with the evolution of drugs to target the synthesis of the protein. AGT is a noninhibitory serpin that has several conserved domains in addition to the angiotensin II sequences at the N terminus. Increased study is needed on the structure-function r...
Source: Arteriosclerosis, Thrombosis and Vascular Biology - April 4, 2024 Category: Cardiology Authors: Alan Daugherty Hisashi Sawada Mary B Sheppard Hong S Lu Source Type: research

Single-Cell RNA Sequencing Reveals an Immune Landscape of CD4 < sup > + < /sup > T Cells in Coronary Culprit Plaques With Acute Coronary Syndrome in Humans
CONCLUSIONS: For the first time, we revealed single cell-level characteristics of CD4+ T cells in patients with ACS. CD4+ T cells could be therapeutic targets of ACS.REGISTRATION: URL: https://www.umin.ac.jp/ctr; Unique identifier: UMIN000040747.PMID:38572648 | DOI:10.1161/ATVBAHA.123.320409 (Source: Arteriosclerosis, Thrombosis and Vascular Biology)
Source: Arteriosclerosis, Thrombosis and Vascular Biology - April 4, 2024 Category: Cardiology Authors: Shintaro Takeda Takuo Emoto Tomoya Yamashita Hiroyuki Yamamoto Tomofumi Takaya Takahiro Sawada Takeshi Yoshida Masatoshi Inoue Yuya Suzuki Tomoyo Hamana Taishi Inoue Masayuki Taniguchi Naoto Sasaki Hiromasa Otake Takenao Ohkawa Tomoyuki Furuyashiki Hiroya Source Type: research