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SM22α-Lineage Perivascular Stromal Cells Contribute to Abdominal Aortic Aneurysm. Circ. Res. (IF 16.5) Pub Date : 2025-05-15 Xiaoxi Pan,Run Zhang,Bingling Lu,Siyuan Chen,Hongjin Chen,Mengyao Li,Le Qin,Zhiyun Song,Yi Yang,Zhe Wang,Fuhua Yan,Aijun Sun,Fang Wu,Lichi Zhang,Jiguang Wang,Tomasz J Guzik,Pingjin Gao
BACKGROUND Perivascular adipose tissue (PVAT) is a key regulator of vascular dysfunction. Impairment of PVAT phenotypic plasticity with aging may play a role in vascular pathology including abdominal aortic aneurysms (AAAs). Yet, the mechanisms underlying PVAT plasticity in aneurysm pathogenesis remain elusive. METHODS Single-cell RNA sequencing was performed on perivascular stromal cells from young
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Rpl13a snoRNAs U34 and U35a: New Targets for Sickle Cell Disease Complications. Circ. Res. (IF 16.5) Pub Date : 2025-05-15 Waseem Chauhan,Sudharshan Setra Janardhana Shetty,Shirin Ferdowsi,Sweta Kafle,Rahima Zennadi
BACKGROUND In sickle cell disease (SCD), erythrocyte reactive oxygen species (ROS) production and oxidative stress play a critical role in vaso-occlusion, a hallmark of SCD. Small noncoding nucleolar RNAs (snoRNAs) of the Rpl13a locus have been described as regulators of ROS levels. However, whether Rpl13a snoRNAs are present in sickle red blood cells (RBCs) and regulate ROS levels and whether they
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Novel Aortic Dissection Model Links Endothelial Dysfunction and Immune Infiltration. Circ. Res. (IF 16.5) Pub Date : 2025-05-14 Kenichi Kimura,Eri Motoyama,Sachiko Kanki,Keiichi Asano,Patrick Sips,Md Al Amin Sheikh,Maria Thea Rane Dela Cruz Clarin,Erna Raja,Mariko Takeda,Ryutaro Ishii,Kazuya Murata,Violette Deleeuw,Laura Muiño Mosquera,Julie De Backer,Seiya Mizuno,Lynn Y Sakai,Tomoyuki Nakamura,Hiromi Yanagisawa
BACKGROUND Aortic dissection (AD) is the separation of medial layers of the aorta and is a major cause of death in patients with connective tissue disorders such as Marfan syndrome. However, molecular triggers instigating AD, its temporospatial progression, and how vascular cells in each vessel layer interact and participate in the pathological process remain incompletely understood. To unravel the
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FoxO1-zDHHC4-CD36 S-Acylation Axis Drives Metabolic Dysfunction in Diabetes. Circ. Res. (IF 16.5) Pub Date : 2025-05-13 Kaitlyn M J H Dennis,Keshav Gopal,Claudia N Montes Aparicio,Jiashuo Aaron Zhang,Marcos Castro-Guarda,Thomas Nicol,Ríona M Devereux,Ryan D Carter,Saara-Anne Azizi,Tong Lan,Ujang Purnama,Carolyn A Carr,Gul Simsek,Eleanor K Gill,Pawel Swietach,Oana Sorop,Ilkka H A Heinonen,Francesco Schianchi,Joost J F P Luiken,Dunja Aksentijevic,Dirk J Dunker,Bryan C Dickinson,Sarah De Val,John R Ussher,William Fuller
BACKGROUND The fatty acid (FA) transporter CD36 (FA translocase/cluster of differentiation 36) is the gatekeeper of cardiac FA metabolism. Preferential localization of CD36 to the sarcolemma is one of the initiating cellular responses in the development of muscle insulin resistance and the type 2 diabetic heart. Posttranslational S-acylation controls protein trafficking, and in this study, we hypothesized
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Acinetobacter Baumannii Secreted Protease CpaA Inhibits Factor XII-Mediated Bradykinin Generation and Neutrophil Activation. Circ. Res. (IF 16.5) Pub Date : 2025-05-13 Kris M Blair,Dillon J Bohinc,Kara L Bane,Mark Warnock,Basel Abuaita,Colby Gura,Eduarda Grinsztejn,Steven H Marshall,Brigid M Wilson,Robert A Bonomo,Ajay Tambralli,Jason S Knight,Mary X O'Riordan,Daniel A Lawrence,Evi X Stavrou,Maria Sandkvist
BACKGROUND FXII (coagulation factor XII) is best known for its roles in the contact and kallikrein-kinin pathways. FXII is converted to its active enzyme (FXIIa [activated factor XII]) by PKa (plasma kallikrein) or its unique ability to autoactivate on bacterial or other biologic surfaces. In vivo, FXIIa initiates the intrinsic coagulation pathway and promotes inflammation by reciprocal activation
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MHCIIhiLYVE1loCCR2hi Interstitial Macrophages Promote Medial Fibrosis in Pulmonary Arterioles and Contribute to Pulmonary Hypertension. Circ. Res. (IF 16.5) Pub Date : 2025-05-13 Fan Qiu,Hao-Ran Miao,Hong-Liang Hui,Lin-Jie Qiu,Yi Chen,Min Luo,Jian-Chao Zhang,Yan-Gui Lin,Dan Li,Sang-Bing Ong,Xue-Fei Hu,Bo Jiang,Yi-Qian Zhang
BACKGROUND Pulmonary hypertension (PH) is a lethal disease characterized in part by progressive pulmonary arteriole (PA) remodeling. Excessive PA fibrosis and macrophage infiltration are often present in PH, but the potential associations are obscure. We investigated the link between interstitial macrophage (iMΦ) infiltration and PA fibrosis in PH and idiopathic pulmonary arterial hypertension. METHODS
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Cell Type-Specific Secretome Analysis Reveals Liver-Heart Crosstalk in HFpEF. Circ. Res. (IF 16.5) Pub Date : 2025-05-12 Jan Philipp Schütte,Nicola Markus,Steve Grein,Verena Kamuf-Schenk,Claudia Stroh,Mandy Rettel,Frank Stein,Johannes Fischer,Zoe Loewenthal,Johannes Leiner,Bing Wang,David M Kaye,Maura M Zylla,Norbert Frey,Mirko Völkers
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Mitochondrial NNT Promotes Diastolic Dysfunction in Cardiometabolic HFpEF. Circ. Res. (IF 16.5) Pub Date : 2025-05-09 Mark E Pepin,Philipp J M Konrad,Sumra Nazir,Farhad Bazgir,Christoph Maack,Alexander Nickel,Joshua Gorman,Mathias Hohl,Friederike Schreiter,Matthias Dewenter,Adriano de Britto Chaves Filho,Almut Schulze,Anja Karlstaedt,Norbert Frey,Christine Seidman,Jonathan Seidman,Johannes Backs
BACKGROUND Clinical management of heart failure with preserved ejection fraction (HFpEF) is hindered by a lack of disease-modifying therapies capable of altering its distinct pathophysiology. Despite the widespread implementation of a 2-hit model of cardiometabolic HFpEF to inform precision therapy, which utilizes ad libitum high-fat diet and 0.5% N(ω)-nitro-L-arginine methyl ester, we observe that
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Intrinsic Ketogenic Capacity of the Heart: Mechanisms and Therapeutic Potential. Circ. Res. (IF 16.5) Pub Date : 2025-05-08 Rosanna Caputo,Carolina Magdalen Greco
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Lymphocyte Failure Drives Pulmonary Vein Remodeling in PH-LHD Models. Circ. Res. (IF 16.5) Pub Date : 2025-05-08 Yann Grobs,Sarah Eve Lemay,Francois Potus
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New Minimally Invasive Myocardial Ischemia/Reperfusion Approach. Circ. Res. (IF 16.5) Pub Date : 2025-05-08 Danielle Altieri,Kristina Lorenz,Slava Epelman
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Value of Bioinformatics Models for Predicting Translational Control of Angiogenesis. Circ. Res. (IF 16.5) Pub Date : 2025-05-08 Michal Shaposhnikov,Juilee Thakar,Bradford C Berk
Angiogenesis, the formation of new blood vessels, is a fundamental biological process with implications for both physiological functions and pathological conditions. While the transcriptional regulation of angiogenesis, mediated by factors such as HIF-1α (hypoxia-inducible factor 1-alpha) and VEGF (vascular endothelial growth factor), is well-characterized, the translational regulation of this process
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Histone Methyltransferase SETD2: A Key Player in Cardiometabolic HFpEF. Circ. Res. (IF 16.5) Pub Date : 2025-05-08 Simone Serio,Roberto Papait
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Circular Tale of Micropeptides in Cardiac Hypertrophy. Circ. Res. (IF 16.5) Pub Date : 2025-05-08 Thierry Pedrazzini
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Pharmacogenomics and Pharmacokinetics of Aspirin in Preeclampsia Prevention. Circ. Res. (IF 16.5) Pub Date : 2025-05-07 Kenean Getaneh Tlaye,Gashaw Garedew Woldeamanuel,Kenneth Chi-Yin Wong,Lu Chen,Ruqun Zheng,Pui Kin So,Xueqin Wang,Long Nguyen-Hoang,Mei Zhong,Hon Cheong So,Bo Wah Leung,Yu Huang,Yao Wang,Liona C Poon,Chi Chiu Wang
BACKGROUND It has become evident that some women develop preeclampsia despite aspirin. This study aimed to examine how such aspirin nonresponsiveness develops in high-risk preeclampsia pregnancies by exploring the role of genetic polymorphisms and aspirin metabolism. METHODS The study involved pregnant women who developed preeclampsia despite low-dose aspirin and those who did not. First, we conducted
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Heart-Brain Crosstalk in Myocardial Infarction: Role of Heart Extracellular Vesicles in Neuroinflammation. Circ. Res. (IF 16.5) Pub Date : 2025-05-01 Ke Liao,Jiayi Yu,Zahra Mohammadigoldar,Junlang Li,Weixin Liu,Liang Li,Eduardo Marbán
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Overload of Neprilysin in Placental Extracellular Vesicles Disrupts CNP-NPRB-Mediated Communication Between Vascular Endothelial and Smooth Muscle Cells: A Trigger for Symptoms of Preeclampsia. Circ. Res. (IF 16.5) Pub Date : 2025-04-30 Chengjin He,Yi Du,Ruixin Chen,Yuhan Qiu,Jiayu Huang,Li Lin,Mark D Kilby,Yong Fu,Hongbo Qi,Philip N Baker,Chao Tong
BACKGROUND Preeclampsia is a placenta-origin pregnancy complication. Although its development has long been divided into 2 stages: abnormal placentation (stage I) and the release of factors from the hypoperfused placenta into circulation, triggering preeclampsia due to endothelial dysfunction (stage II), the placenta-derived substances coupling the 2 stages remain unclear. METHODS Extracellular vesicles
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Habitual Exercise Modulates Neuroimmune Interaction to Mitigate Aortic Stiffness. Circ. Res. (IF 16.5) Pub Date : 2025-04-30 Jae Min Cho,Khoa Vu,Seul-Ki Park,Enbo Zhu,Yan-Ruide Li,Peng Zhao,Tomohiro Yokota,Lili Yang,Rong Lu,Yang Kevin Xiang,Ying H Shen,Mark W Chapleau,Tzung K Hsiai
BACKGROUND Exercise augments hemodynamic shear to activate mechano-sensitive molecular transducers in the vascular endothelium. Recently, the central nervous system has been reported to mediate neuroimmune interaction in the aortic adventitia (AA). Whether exercise modulates the sympathetic nerve interaction with the immune cells to mitigate aortic stiffness remains unknown. METHODS AND RESULTS Four
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Endothelial KLF15/VASN Axis Inhibits Angiogenesis via Activation of Notch1 Signaling. Circ. Res. (IF 16.5) Pub Date : 2025-04-29 Jia Zhang,Jia-Jia Zhao,Han-Dan Zhou,Jing Chen,Mo-Na Hong,Ji-Guang Wang,Ping-Jin Gao,Xiao-Dong Li
BACKGROUND Angiogenesis is a dynamic process fine-tuned by transcription factors in endothelial cells. The KLF15 (Krüppel-like factor 15)-mediated transcriptional regulation mechanism is critical for cardiovascular diseases. However, the role of KLF15 in governing angiogenesis remains unknown. METHODS KLF15 and VASN (vasorin) were deleted from endothelial cells using tamoxifen-inducible Cdh5 promoter-driven
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Natural Killer T Cells Link Stress Hyperglycemia to Cognitive Decline in HFpEF. Circ. Res. (IF 16.5) Pub Date : 2025-04-28 Pasquale Mone,Michele Ciccarelli,Stanislovas S Jankauskas,Francesca Picone,Germano Guerra,Gianluca Testa,Francesco Moccia,Roberto Magliuolo,Marco Di Mauro,Antonio De Luca,Albino Carrizzo,Carmine Vecchione,Gaetano Santulli
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MAIT Cells in Lipoprotein Metabolism: A New Pathway for VLDL Clearance? Circ. Res. (IF 16.5) Pub Date : 2025-04-24 Majid M Syed-Abdul,Gary F Lewis
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Thyroid Hormone Signaling in Cerebrovascular Malformations: A Regulator of Vascular Stability and Repair. Circ. Res. (IF 16.5) Pub Date : 2025-04-24 Seokhyun Kim,Minho Shong,Injune Kim
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Impact of Cholesterol on Cardiac Mitochondrial Function. Circ. Res. (IF 16.5) Pub Date : 2025-04-24 Gary D Lopaschuk
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Stellate Ganglia: A Key Therapeutic Target for Malignant Ventricular Arrhythmia in Heart Disease. Circ. Res. (IF 16.5) Pub Date : 2025-04-24 Yu-Long Li,Yu Li,Huiyin Tu,Anthony J Evans,Tapan A Patel,Hong Zheng,Kaushik P Patel
Malignant ventricular arrhythmias (VAs), such as ventricular tachycardia and ventricular fibrillation, are the cause of approximately half a million deaths per year in the United States, which is a common lethal event in heart disease, such as hypertension, catecholaminergic polymorphic ventricular tachycardia, takotsubo cardiomyopathy, long-QT syndrome, and progressing into advanced heart failure
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Novel Humanized Aortic Valve Calcification Model. Circ. Res. (IF 16.5) Pub Date : 2025-04-24 Dunpeng Cai,Lindsey Saint,John Markley,Shi-You Chen
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Tracking Endothelial Extracellular Vesicles in a Mouse Model of Atherosclerosis. Circ. Res. (IF 16.5) Pub Date : 2025-04-23 Mandy Kunze Guo,Corey A Scipione,Leandro C D Breda,Kamalben Prajapati,Sneha Raju,Steven R Botts,Majed Abdul-Samad,Sarvatit Patel,Garry Yu,Andrew C Dudley,Jason E Fish,Kathryn L Howe
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Reducing Granules Without Splicing Restoration Alleviates RBM20 Cardiomyopathy. Circ. Res. (IF 16.5) Pub Date : 2025-04-17 Mei Methawasin,Yanghai Zhang,Zachery R Gregorich,Yaqin He,Chunling Liu,Julia Muldoon,Zaynab Hourani,John E Smith,Henk Granzier,Wei Guo
BACKGROUND RBM20 (RNA binding motif protein 20) cardiomyopathy is a severe form of dilated cardiomyopathy (DCM). Genetic variants in the nuclear localization signal of Rbm20 hinder its nuclear import and promote cytoplasmic pathogenic RNP (ribonucleoprotein) granules. We aimed to investigate whether reducing RNP granules by inhibiting Rbm20 expression could alleviate the DCM phenotype in Rbm20 S639G
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Novel Truncated Peptide Derived From circCDYL Exacerbates Cardiac Hypertrophy. Circ. Res. (IF 16.5) Pub Date : 2025-04-17 Mengyang Li,Wei Ding,Xinyu Fang,Yu Wang,Peiyan Wang,Lin Ye,Shuo Miao,Lin Song,Xiang Ao,Qi Li,Jianxun Wang
BACKGROUND Circular RNAs (circRNAs) have been gradually revealed to regulate the progression of heart disease in depth, showing their clinical significance. However, a mass of cardiac circRNAs still has not been functionally characterized. We aimed to explore the potential candidates that are involved in pathological cardiac hypertrophy. METHODS Public substantial RNA-sequencing data of cardiac circRNAs
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Treg Cells Attenuate Pulmonary Venous Remodeling in PH-LHD via NLRC3 Signaling. Circ. Res. (IF 16.5) Pub Date : 2025-04-16 Gulinigeer Zhakeer,Yanxi Zeng,Guangxi E,Nuerbiyemu Maimaitiaili,Peinan Ju,Hongyun Yao,Yefei Shi,Ming Zhai,Ke Li,Jianhui Zhuang,Yunshan Cao,Qing Yu,Wenhui Peng
BACKGROUND Pulmonary venous remodeling is a key pathological feature of pulmonary hypertension associated with left heart disease (PH-LHD). This study aims to investigate the role of regulatory T (Treg) cells in this process. METHODS We used mouse models with transverse aortic constriction and cell depletion of Foxp3-DTR/tdTomato mice to examine Treg cells' function around pulmonary veins in PH-LHD
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The Heart Has Intrinsic Ketogenic Capacity that Mediates NAD+ Therapy in HFpEF. Circ. Res. (IF 16.5) Pub Date : 2025-04-11 Yen Chin Koay,Bailey McIntosh,Yann Huey Ng,Yang Cao,Xiao Suo Wang,Yanchuang Han,Saki Tomita,Angela Yu Bai,Benjamin Hunter,Ashish Misra,Christopher M Loughrey,Paul G Bannon,Sean Lal,Aldons J Lusis,David M Kaye,Mark Larance,John F O'Sullivan
BACKGROUND Heart failure with preserved ejection fraction (HFpEF) has overtaken heart failure with reduced ejection fraction as the leading type of heart failure globally and is marked by high morbidity and mortality rates, yet with only a single approved pharmacotherapy: SGLT2i (sodium-glucose co-transporter 2 inhibitor). A prevailing theory for the mechanism underlying SGLT2i is nutrient deprivation
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Chromatin Rewiring by SETD2 Drives Lipotoxic Injury in Cardiometabolic HFpEF. Circ. Res. (IF 16.5) Pub Date : 2025-04-11 Sarah Costantino,Shafeeq A Mohammed,Samuele Ambrosini,Marialucia Telesca,Alessandro Mengozzi,Kaivalya Walavalkar,Era Gorica,Melissa Herwig,Loek van Heerebeek,Junyan Xia,Gergely Karsai,Thorsten Hornemann,Omer Dzemali,Raffaella Santoro,Qian Lin,Frank Ruschitzka,Nazha Hamdani,Francesco Paneni
BACKGROUND Cardiometabolic heart failure with preserved ejection fraction (cHFpEF) is a highly prevalent and deadly condition. Histone 3 trimethylation at lysine 36 (H3k36me3)-a chromatin signature induced by the histone methyltransferase SETD2 (SET domain containing 2)-correlates with changes in gene expression in human failing hearts; however, its role remains poorly understood. This study investigates
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Long Noncoding RNA MIR181A1HG Takes a Proinflammatory Driver's Seat in Atherosclerosis by Hijacking FOXP1. Circ. Res. (IF 16.5) Pub Date : 2025-04-10 James A Oo,Timothy Warwick,Matthias S Leisegang
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TMEM-ing the Tide: Gene Therapy Holds Promise for ARVC5. Circ. Res. (IF 16.5) Pub Date : 2025-04-10 Sandra Ratnavadivel,Matthew W Ellis,Farah Sheikh
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Gut Instincts: The Gut Microbiome-Cardiovascular Inflammation Axis. Circ. Res. (IF 16.5) Pub Date : 2025-04-10 Jessie M Dalman,Emma R Blaustein,Coen van Solingen
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Nuclear Receptors in Platelet Activation and Thrombosis in Hypercholesterolemia. Circ. Res. (IF 16.5) Pub Date : 2025-04-10 Yanki Yarman,Xuefei Zhao,Peisong Ma
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Pathways and Molecular Mechanisms Governing LDL Receptor Regulation. Circ. Res. (IF 16.5) Pub Date : 2025-04-10 Heidi M Schmidt,Kelsey E Jarrett,Thomas Q de Aguiar Vallim,Elizabeth J Tarling
Clearance of circulating plasma LDL (low-density lipoprotein) cholesterol by the liver requires hepatic LDLR (low-density lipoprotein receptor). Complete absence of functional LDLR manifests in severe hypercholesterolemia and premature atherosclerotic cardiovascular disease. Since the discovery of the LDLR 50 years ago by Brown and Goldstein, all approved lipid-lowering medications have been aimed
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High-Throughput Echocardiography-Guided Induction of Myocardial Ischemia/Reperfusion in Mice. Circ. Res. (IF 16.5) Pub Date : 2025-04-10 Florian Sicklinger,Niklas Hartmann,Attila Kovacs,Carla Weinheimer,Jess Nigro,Tobias Thiemann,Junedh M Amrute,David Schumacher,Moritz P Kornadt,Laura M Wienecke,Lennart Rompel,Johannes Fischer,John Bachman,Olivia Bedard,Shibali Das,Tim C Kuhn,Mirko Völkers,Ralf P Brandes,Rafael Kramann,Nadia Rosenthal,Norbert Frey,Kory J Lavine,Florian Leuschner
BACKGROUND Mouse models of myocardial ischemia with subsequent heart failure are common approaches to examine heart failure pathology and possible treatment strategies. We sought to establish a high-throughput approach for echocardiography-guided induction of myocardial ischemia/reperfusion (IR) in mice. METHODS After visualization of the left coronary artery with high-resolution ultrasound imaging
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Metabolic Coordination Structures Contribute to Diabetic Myocardial Dysfunction. Circ. Res. (IF 16.5) Pub Date : 2025-04-07 Teng Wu,Tongsheng Huang,Honglin Ren,Conghui Shen,Jiang Qian,Xinlu Fu,Shangyuan Liu,Chengshu Xie,Xi Lin,Junhong Wan,Shijie Xiong,Yuanjun Ji,Mengying Liu,Huiting Zheng,Ting Liang,Wenyi Liu,Yan Zou,Kingwai Lai,Maoquan Yang,Zeyi Song,Peixuan Lan,Xinghui Li,Yandi Wu,Ming Yang,Hui Li,Xuezhe Huang,Hui Chen,Jing Tan,Weibin Cai
BACKGROUND Individuals with diabetes are susceptible to cardiac dysfunction and heart failure, potentially resulting in mortality. Metabolic disorders frequently occur in patients with diabetes, and diabetes usually leads to remodeling of heart structure and cardiac dysfunction. However, the contribution and underlying mechanisms of metabolic and structural coupling in diabetic cardiac dysfunction
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Piezo1 in PASMCs: Critical for Hypoxia-Induced Pulmonary Hypertension Development. Circ. Res. (IF 16.5) Pub Date : 2025-04-04 Fenja Knoepp,Shariq Abid,Amal Houssaini,Larissa Lipskaia,Mira Yasemin Gökyildirim,Emmanuelle Born,Elisabeth Marcos,Malika Arhatte,Edyta Glogowska,Nora Vienney,Andreas Günther,Simone Kraut,Ingrid Breitenborn-Mueller,Karin Quanz,Dagmar Fenner-Nau,Geneviève Derumeaux,Norbert Weissmann,Eric Honoré,Serge Adnot
BACKGROUND Pulmonary hypertension (PH) is a life-threatening and progressive yet incurable disease. The hallmarks of PH comprise (1) sustained contraction and (2) excessive proliferation of pulmonary arterial smooth muscle cells (PASMCs). A major stimulus to which PASMCs are exposed during PH development is altered mechanical stress, originating from increased blood pressure, changes in blood flow
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PCSK9 Regulates Cardiac Mitochondrial Cholesterol by Promoting TSPO Degradation. Circ. Res. (IF 16.5) Pub Date : 2025-04-02 Marion Laudette,Malin Lindbom,Mathieu Cinato,Per-Olof Bergh,Kristina Skålén,Muhammad Arif,Azra Miljanovic,Tomasz Czuba,Rosie Perkins,J Gustav Smith,Frank Lezoualc'h,Malin C Levin,Jan Borén
BACKGROUND Cholesterol is critical for mitochondrial membrane structure and function. Given the emergence of mitochondria as a key factor in the pathogenesis of heart failure, mitochondrial cholesterol homeostasis may be crucial for maintaining mitochondrial properties and thus cardiac function. We previously showed that CM-Pcsk9-/- mice (mice with cardiomyocyte-specific deletion of the gene encoding
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Srsf3-Dependent APA Drives Macrophage Maturation and Limits Atherosclerosis. Circ. Res. (IF 16.5) Pub Date : 2025-03-31 Xian Yang,Xin Zhang,Yaru Tian,Jiaxuan Yang,Yunhui Jia,Yuhuai Xie,Lianping Cheng,Shenglai Chen,Linfeng Wu,Yihong Qin,Zhen Zhao,Dejian Zhao,Yuanyuan Wei
BACKGROUND Circulating monocytes largely contribute to macrophage buildup in atheromata, which is crucial for clearing subendothelial LDLs (low-density lipoproteins) and dead cells; however, the transitional trajectory from monocytes to macrophages in atherosclerotic plaques and the underlying regulatory mechanism remain unclear. Moreover, the role of alternative polyadenylation, a posttranscriptional
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Stop Me at Your Own PeRiL: PRL2 Constrains AMPK in the Pressure-Overloaded Heart. Circ. Res. (IF 16.5) Pub Date : 2025-03-27 Edoardo Bertero,Alessandra Ghigo,Pietro Ameri
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Cardiac Fibrosis in the Multi-Omics Era: Implications for Heart Failure. Circ. Res. (IF 16.5) Pub Date : 2025-03-27 Rachad Ghazal,Min Wang,Duan Liu,Daniel J Tschumperlin,Naveen L Pereira
Cardiac fibrosis, a hallmark of heart failure and various cardiomyopathies, represents a complex pathological process that has long challenged therapeutic intervention. High-throughput omics technologies have begun revolutionizing our understanding of the molecular mechanisms driving cardiac fibrosis and are providing unprecedented insights into its heterogeneity and progression. This review provides
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Taxing Hearts: TAX1BP3 Loss Stirs Up TRPV4 Channels in Arrhythmogenic Cardiomyopathy. Circ. Res. (IF 16.5) Pub Date : 2025-03-27 Sandra Ratnavadivel,Afaf Jreije,Farah Sheikh
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Biophysical and Biochemical Roles of Shear Stress on Endothelium: A Revisit and New Insights. Circ. Res. (IF 16.5) Pub Date : 2025-03-27 Chak Kwong Cheng,Nanping Wang,Li Wang,Yu Huang
Hemodynamic shear stress, the frictional force exerted by blood flow on the endothelium, mediates vascular homeostasis. This review examines the biophysical nature and biochemical effects of shear stress on endothelial cells, with a particular focus on its impact on cardiovascular pathophysiology. Atherosclerosis develops preferentially at arterial branches and curvatures, where disturbed flow patterns
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MAIT Cells Promote Cholesterol Excretion Pathways Mitigating Atherosclerosis. Circ. Res. (IF 16.5) Pub Date : 2025-03-26 Hua Wang,Pukar Kc,Kaidi Zhang,Clément Materne,Marie Lhomme,Sophie Galier,Farid Ichou,Carolina Neves,Agnès Lehuen,Joel T Haas,Joe-Elie Salem,Maryse Guerin,Philippe Lesnik
BACKGROUND Previous clinical studies have indicated reduced circulating mucosal-associated invariant T (MAIT) cells in individuals with coronary artery disease. However, the precise role and underlying mechanisms of MAIT cells in this context remain unclear. Immune homeostasis plays a pivotal role in the development of atherosclerosis. This study explores the impact of MAIT cells on atherosclerosis
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Local DIO2 Elevation Is an Adaption in Malformed Cerebrovasculature. Circ. Res. (IF 16.5) Pub Date : 2025-03-25 Ruofei Li,Yushan Tang,Haiyue Wang,Pengyan Hu,Liang Yu,Cheng Lv,Yu Zhang,A Martin Gerdes,Yibo Wang
BACKGROUND Cerebrovascular malformations are a pivotal cause of hemorrhage and neurological disability alongside lacking effective medication. Thyroid hormones (THs), including thyroxine and triiodothyronine, are essential for vascular development, yet whether they participate in malformed cerebrovascular pathology remains elusive. METHODS Single-cell transcriptome analysis characterized human cerebral
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Overexpression of Wild-Type TMEM43 Improves Cardiac Function in Arrhythmogenic Right Ventricular Cardiomyopathy Type 5. Circ. Res. (IF 16.5) Pub Date : 2025-03-17 Laura Lalaguna,María Arévalo-Núñez de Arenas,Marina López-Olañeta,María Villalba-Orero,Rafael J Jiménez-Riobóo,María Victoria Gómez-Gaviro,Joan Isern,Pura Muñoz-Cánoves,Barry J Byrne,Juan Pablo Ochoa,Pablo García-Pavía,Enrique Lara-Pezzi
BACKGROUND Arrhythmogenic right ventricular cardiomyopathy type 5 (ARVC5) is the most aggressive type of ARVC, caused by a fully penetrant missense mutation (p.S358L) in TMEM43 (transmembrane protein 43). Pathologically, the disease is characterized by dilation of the cardiac chambers and fibrofatty replacement of the myocardium, which results in heart failure and sudden cardiac death. Current therapeutic
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Introduction to the Compendium on Lifelong Care in Women: Applying a Sex- and Gender-Lens to Practice. Circ. Res. (IF 16.5) Pub Date : 2025-03-13 Kathryn J Lindley
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Understanding Thoracic Aortic Disease in Women. Circ. Res. (IF 16.5) Pub Date : 2025-03-13 Bana Samman,Mimi X Deng,Jennifer C Y Chung,Maral Ouzounian
Multifaceted disparities exist between men and women with thoracic aortic aneurysm and dissection. Despite a higher prevalence of thoracic aortic aneurysm and dissection among men, women experience disproportionately accelerated aneurysmal expansion, greater risks of rupture or dissection, and acute aortic syndromes that occur at relatively smaller diameters. In the context of acute type A aortic dissection
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Strategies for Overcoming Barriers in Access to Cardiovascular Care for Women. Circ. Res. (IF 16.5) Pub Date : 2025-03-13 Deirdre J Mattina,Michael C Honigberg,Zainab Mahmoud,Karen E Joynt Maddox
Women face unique barriers to equitable health care. To ensure access to quality cardiovascular care across the lifespan of women, several systemic and social challenges need to be addressed. With the understanding that women often direct health care decisions, not only for themselves but for their family unit as well, a holistic approach to address health care barriers is warranted. This review aims
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The 2024 US Medical Eligibility Criteria for Contraceptive Use: Application to Practice in the Care of Patients With Cardiac Disease. Circ. Res. (IF 16.5) Pub Date : 2025-03-13 Kayle Shapero,Tessa Madden
Cardiovascular disease is the leading cause of maternal mortality in the United States, with the majority of deaths stemming from preventable causes. Contraception is one of the tools that can be utilized to prevent mortality and morbidity associated with unplanned pregnancy in patients with underlying congenital or acquired heart disease. There are a wide range of contraceptive methods available.
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Lifelong Care of Females With Congenital Heart Disease. Circ. Res. (IF 16.5) Pub Date : 2025-03-13 Rose Tompkins,Prashanth Venkatesh,Adam J Small,Dan G Halpern
Medical and surgical advancements of the past 70 years have resulted in a remarkable shift in the natural history of congenital heart disease (CHD) such that survival to adulthood is expected for >90% of children born with congenital heart defects, including those with complex CHD. There are now more adults than children living with CHD, a majority of them are female. As significant strides have been
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Influence of Primary Neurologic Disease on Cardiovascular Health in Females. Circ. Res. (IF 16.5) Pub Date : 2025-03-13 Khadija Awais Ali,Deborah L G Kerrigan,Jillian Molli Berkman
Neurocardiology is an interdisciplinary field that examines the complex interactions between the nervous and the cardiovascular systems, exploring how neurological processes, such as autonomic nervous system regulation and brain-heart communication impact heart function and contribute to cardiovascular health and disease. Although much of the focus on cardiovascular health has centered on traditional
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Advances in Our Understanding of Cardiovascular Diseases After Preeclampsia. Circ. Res. (IF 16.5) Pub Date : 2025-03-13 Malamo E Countouris,Natalie A Bello
Preeclampsia is a syndrome of hypertension in association with target organ dysfunction, including proteinuria, which manifests during pregnancy and the immediate postpartum period. The pathophysiology of preeclampsia originates from impaired trophoblastic invasion of the placental resulting in malperfusion and involves multiple mechanistic pathways that include anti-angiogenic factors, endothelial
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Sex-Specific Factors Influencing Obesity in Women: Bridging the Gap Between Science and Clinical Practice. Circ. Res. (IF 16.5) Pub Date : 2025-03-13 Hazem Ayesh,Samar A Nasser,Keith C Ferdinand,Barbara Gisella Carranza Leon
Obesity in women is a significant public health issue with serious implications for cardiovascular-kidney-metabolic syndrome and cardiovascular disease. This complex challenge is influenced by physiological, hormonal, socioeconomic, and cultural factors. Women face unique weight management challenges due to hormonal changes during pregnancy, perimenopause, and menopause, which affect fat distribution
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March2 Alleviates Aortic Aneurysm/Dissection by Regulating PKM2 Polymerization. Circ. Res. (IF 16.5) Pub Date : 2025-03-13 Yiran E Li,Shuolin Liu,Litao Wang,Yuxin Du,Lin Wu,Haoran Chen,Tingfang Zhu,Jie Lin,Shengjun Xiong,Yayu Wang,Qijun Zheng,Rongjun Zou,Ling Lin,Zheyun Li,Lixin Wang,Junbo Ge,Jun Ren,Yingmei Zhang
BACKGROUND Aortic aneurysm/dissection (AAD) is a life-threatening disease lacking effective pharmacological treatment. Protein ubiquitination plays a pivotal role in cardiovascular diseases. However, the possible contribution of the E3 ubiquitin ligase March2 (membrane-associated RING [really interesting new gene] finger protein 2) to the cause of AAD remains elusive. METHODS Integrated single-cell
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Endothelial Serotonin Receptor 1B Acts as a Mechanosensor to Drive Atherosclerosis. Circ. Res. (IF 16.5) Pub Date : 2025-03-12 Minchun Jiang,Huanyu Ding,Yuhong Huang,Chi Wai Lau,Ying Guo,Jianfang Luo,Yu-Tsung Shih,Yin Xia,Xiaoqiang Yao,Jeng-Jiann Chiu,Li Wang,Shu Chien,Yu Huang
BACKGROUND Atherosclerosis is characterized by the accumulation of fatty and fibrotic plaques, which preferentially develop at curvatures and branches along the arterial trees that are exposed to disturbed flow. However, the mechanisms by which endothelial cells sense disturbed flow are still unclear. METHODS The partial carotid ligation mouse model was used to investigate disturbed flow-induced atherogenesis
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LncRNA MIR181A1HG Deficiency Attenuates Vascular Inflammation and Atherosclerosis. Circ. Res. (IF 16.5) Pub Date : 2025-03-06 Huaner Ni,Yulong Ge,Ying Zhuge,Xiaoqiang Liu,Hangwei Chen,Junyi Liu,Weifeng Li,Xiang Wang,Gu Shen,Qiuling Wang,Rulin Zhuang,Mark W Feinberg,Fang Wang
BACKGROUND Endothelial cell (EC) dysfunction and vascular inflammation are critical in the initiation and progression of atherosclerosis. Long noncoding RNAs play a critical role in vascular pathology, but relatively little is known about their involvement in controlling vascular inflammation. MIR181A1HG is a conserved long noncoding RNA located in juxtaposition with miR-181a1 and miR-181b1, both involved
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NR4A1 Acts as a Novel Regulator of Platelet Activation and Thrombus Formation. Circ. Res. (IF 16.5) Pub Date : 2025-03-04 Wenhua Liu,Gaoxiang Li,Jianfeng Shi,Yu Gao,Peiliang Fang,Yichao Zhao,Fangyuan Zhong,Xiao Guo,Yuyan Lyu,Xingwen Da,Zhaoyan Li,Jingjing Fa,Liuhua Hu,Ancai Yuan,Lei Chen,Junling Liu,Alex F Chen,Bin Sheng,Yong Ji,Xiyuan Lu,Jun Pu
BACKGROUND Mounting evidence indicates that nuclear receptors play a critical regulatory role in platelet pathophysiology and thrombotic disorders. Although NR4A (the nuclear receptor subfamily 4 group A) plays an important role in cardiovascular pathophysiology, the expression profile and biological function of NR4A member 1 (NR4A1) in platelets have never been reported. METHODS We evaluated the functions