Circulation research最新文献

{"title":"ACKR1^hiECs Promote Aortic Dissection Through Adjusting Macrophage Behavior.","authors":"Yayu Wang, Xiong Jia, Yifei Zhang, Bin Zhang, Yazhe Zhou, Xiaoru Li, Xiaoying Zhu, Jinquan Xia, Jun Ren, Chang Zou, Qijun Zheng","doi":"10.1161/CIRCRESAHA.124.325458","DOIUrl":"https://doi.org/10.1161/CIRCRESAHA.124.325458","url":null,"abstract":"<p><strong>Background: </strong>Type A aortic dissection (TAAD) is a life-threatening condition characterized by complex pathophysiology, in which macrophages play a critical but not yet fully understood role. This study focused on the role of endothelial cells with elevated expression of ACKR1 (atypical chemokine receptor 1) and their interaction with proinflammatory macrophages in TAAD development.</p><p><strong>Methods and results: </strong>Single-cell transcriptomic analysis of human aortic tissues revealed increased populations of endothelial cells exhibiting high ACKR1 expression and proinflammatory macrophages in TAAD samples. Both clinical and animal studies revealed that ACKR1 expression levels were strongly linked to TAAD severity. Gain- and loss-of-function studies demonstrated that ACKR1 promotes TAAD progression. Specific knockdown of ACKR1 in endothelial cells suppressed the NF-κB (nuclear factor-κB) signaling pathway and SPP1 (secreted phosphoprotein 1) expression, leading to reduced macrophage migration and proinflammatory polarization, which subsequently inhibited TAAD development. Conversely, ACKR1 overexpression accelerated TAAD progression. Notably, molecular docking and comprehensive evaluation identified amikacin as a potential novel modulator of ACKR1. Extensive in vitro and in vivo studies demonstrated that amikacin can regulate macrophage behavior through the ACKR1/NF-κB/SPP1 signaling pathway, thereby attenuating TAAD progression and improving survival rates in TAAD mice.</p><p><strong>Conclusions: </strong>This study reveals how endothelial cells exhibiting high ACKR1 expression modulate macrophage migration and proinflammatory polarization through the ACKR1/NF-κB/SPP1 signaling pathway, a crucial mechanism in TAAD progression. Targeting ACKR1 through both functional and pharmacological approaches effectively suppressed TAAD progression and extended survival in TAAD mice, offering promising new intervention strategies for clinical evaluation.</p>","PeriodicalId":10147,"journal":{"name":"Circulation research","volume":" ","pages":""},"PeriodicalIF":16.5,"publicationDate":"2024-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142845855","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Follistatin From hiPSC-Cardiomyocytes Promotes Myocyte Proliferation in Pigs With Postinfarction LV Remodeling.","authors":"Yuhua Wei, Gregory Walcott, Thanh Nguyen, Xiaoxiao Geng, Bijay Guragain, Hanyu Zhang, Akazha Green, Manuel Rosa-Garrido, Jack M Rogers, Daniel J Garry, Lei Ye, Jianyi Zhang","doi":"10.1161/CIRCRESAHA.124.325562","DOIUrl":"https://doi.org/10.1161/CIRCRESAHA.124.325562","url":null,"abstract":"<p><strong>Background: </strong>When human induced pluripotent stem cells (hiPSCs) that CCND2-OE (overexpressed cyclin-D2) were differentiated into cardiomyocytes (^CCND2-OEhiPSC-CMs) and administered to the infarcted hearts of immunodeficient mice, the cells proliferated after administration and repopulated >50% of the scar. Here, we knocked out human leukocyte antigen class I and class II expression in ^CCND2-OEhiPSC-CMs (^KO/OEhiPSC-CMs) to reduce the cells' immunogenicity and then assessed the therapeutic efficacy of ^KO/OEhiPSC-CMs for the treatment of myocardial infarction.</p><p><strong>Methods: </strong>^KO/OEhiPSC-CM and wild-type hiPSC-CM (^WThiPSC-CM) spheroids were differentiated in shaking flasks, purified, characterized, and intramyocardially injected into pigs after ischemia/reperfusion injury; control animals were injected with basal medium. Cardiac function was evaluated via cardiac magnetic resonance imaging, and cardiomyocyte proliferation was assessed via immunostaining and single-nucleus RNA sequencing.</p><p><strong>Results: </strong>Measurements of cardiac function and scar size were significantly better in pigs treated with ^KO/OEhiPSC-CM spheroids than in animals treated with medium or ^WThiPSC-CM spheroids. ^KO/OEhiPSC-CMs were detected for just 1 week after administration, but assessments of cell cycle activity and proliferation were significantly higher in the endogenous pig cardiomyocytes of the hearts from the ^KO/OEhiPSC-CM spheroid group than in those from the other 2 groups. Single-nucleus RNA-sequencing analysis identified a cluster of proliferating cardiomyocytes that was significantly more prevalent in the ^KO/OEhiPSC-CM spheroid-treated hearts (3.65%) than in the hearts from the medium (0.89%) or ^WThiPSC-CM spheroid (1.33%) groups at week 1. YAP (Yes-associated protein) protein levels and nuclear localization were also significantly upregulated in pig cardiomyocytes after treatment with ^KO/OEhiPSC-CM spheroids. Follistatin, which interacts with the HIPPO/YAP pathway, was significantly more abundant in the medium from ^KO/OEhiPSC-CM spheroids than ^WThiPSC-CM spheroids (30.29±2.39 versus 16.62±0.83 ng/mL, <i>P</i>=0.0056). Treatment with follistatin increased ^WThiPSC-CM cell counts by 28.3% over 16 days in culture and promoted cardiomyocyte proliferation in the infarcted hearts of adult mice.</p><p><strong>Conclusions: </strong>^KO/OEhiPSC-CM spheroids significantly improved cardiac function and reduced infarct size in pig hearts after ischemia/reperfusion injury by secreting follistatin, which upregulated HIPPO/YAP signaling and proliferation in endogenous pig cardiomyocytes.</p>","PeriodicalId":10147,"journal":{"name":"Circulation research","volume":" ","pages":""},"PeriodicalIF":16.5,"publicationDate":"2024-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142845859","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SGLT2 Inhibition Induces Cardioprotection by Increasing Parasympathetic Activity.","authors":"Maryna V Basalay, Alla Korsak, Zhenhe He, Alexander V Gourine, Sean M Davidson, Derek M Yellon","doi":"10.1161/CIRCRESAHA.124.324708","DOIUrl":"https://doi.org/10.1161/CIRCRESAHA.124.324708","url":null,"abstract":"","PeriodicalId":10147,"journal":{"name":"Circulation research","volume":" ","pages":""},"PeriodicalIF":16.5,"publicationDate":"2024-12-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142845861","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ET-3/ETBR Mediates Na⁺-Activated Immune Signaling and Kidney Lymphatic Dynamics.","authors":"Ashley L Mutchler, Jianyong Zhong, Hai-Chun Yang, Shilin Zhao, Rachelle Crescenzi, Shannon Taylor, Roy L Rao, Elaine L Shelton, Annet Kirabo, Valentina Kon","doi":"10.1161/CIRCRESAHA.124.324890","DOIUrl":"https://doi.org/10.1161/CIRCRESAHA.124.324890","url":null,"abstract":"<p><strong>Background: </strong>Lymphatic collecting vessels in the kidney are critical in clearing interstitial fluid, macromolecules, and infiltrating immune cells. Dysfunction of the lymphatic vessels can disrupt this process and exacerbate injury-associated inflammation in many disease conditions. We previously found that sodium accumulates within the kidney interstitium during proteinuric kidney injury and elevated sodium environments stimulate isolevuglandin production in antigen-presenting cells, stimulating T cells, and modulating inflammatory responses. In the present study, we investigated whether proteinuric injury increases production of isolevuglandin-adduct formation in antigen-presenting cells, their effects on lymphatic endothelial cells (LECs), and the role of the ET-3 (endothelin-3)/ETBR (endothelin type B receptor) on lymphatic vessel function.</p><p><strong>Methods: </strong>We used a mouse model of nephrotoxin-induced proteinuric injury to show that proteinuric injury expanded the kidney lymphatic network and to immunophenotype the infiltrating immune cells. To determine mechanisms, we analyzed the interaction of migratory immune cells and LECs using an in vitro transwell migration assay, bulk RNA sequencing, and flow cytometric analysis. To determine the effect of ET-3/ETBR axis on lymphatic vessel contractility, we analyzed microdissected lymphangions utilizing a vessel perfusion chamber.</p><p><strong>Results: </strong>We found that animals with proteinuric injury have increased kidney lymphangiogenesis, isolevuglandin-producing dendritic cells, and IFN (interferon)-γ-producing CD4+T cells. The sodium avid environment present in kidney injury enhances the interaction between LECs and migratory antigen-presenting cells and LEC production of isolevuglandin-adducts. Elevated sodium environment-induced isolevuglandin-adduct formation facilitates the ET-3/ETBR communication between LECs and dendritic cells. In addition, the ET-3/ETBR axis modulates lymphatic collecting vessel pumping dynamics.</p><p><strong>Conclusions: </strong>These findings reveal a novel mechanism linking the isolevuglandin-mediated ET-3/ETBR axis with LECs and infiltrating dendritic cells. ET-3/ETBR signaling in lymphatic vessel dynamics is a novel pathogenic component and a possible therapeutic target in kidney disease.</p>","PeriodicalId":10147,"journal":{"name":"Circulation research","volume":" ","pages":""},"PeriodicalIF":16.5,"publicationDate":"2024-12-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142827507","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Endothelial FUNDC1 Deficiency Drives Pulmonary Hypertension.","authors":"Yandong Pei, Dongfeng Ren, Yuanhao Yin, Jiajia Shi, Qianyuan Ai, Wenxin Hao, Xiaofan Luo, Chenyue Zhang, Yanping Zhao, Chenyu Bai, Lin Zhu, Qiong Wang, Shuangling Li, Yuwei Zhang, Jiangtao Lu, Lin Liu, Lin Zhou, Yuli Wu, Yiqi Weng, Yongle Jing, Chengzhi Lu, Yujie Cui, Hao Zheng, Yanjun Li, Guo Chen, Gang Hu, Quan Chen, Xudong Liao","doi":"10.1161/CIRCRESAHA.124.325156","DOIUrl":"https://doi.org/10.1161/CIRCRESAHA.124.325156","url":null,"abstract":"<p><strong>Background: </strong>Pulmonary hypertension (PH) is associated with endothelial dysfunction. However, the cause of endothelial dysfunction and its impact on PH remain incompletely understood. We aimed to investigate whether the hypoxia-inducible FUNDC1 (FUN14 domain-containing 1)-dependent mitophagy pathway underlies PH pathogenesis and progression.</p><p><strong>Methods: </strong>We first analyzed FUNDC1 protein levels in lung samples from patients with PH and animal models. Using rodent PH models induced by HySu (hypoxia+SU5416) or chronic hypoxia, we further investigated PH pathogenesis and development in response to global and cell-type-specific <i>Fundc1</i> loss/gain-of-function. We also investigated the spontaneous PH in mice with inducible loss of endothelial <i>Fundc1</i>. In addition, histological, metabolic, and transcriptomic studies were performed to delineate molecular mechanisms. Finally, findings were validated in vivo by compound deficiency of HIF2α (hypoxia-inducible factor 2α; <i>Epas1</i>) and pharmacological intervention.</p><p><strong>Results: </strong>FUNDC1 protein levels were reduced in PH lung vessels from clinical subjects and animal models. Global <i>Fundc1</i> deficiency exacerbated PH, while its overexpression is protective. The effect of FUNDC1 was mediated by endothelial cells rather than smooth muscle cells. Further, inducible loss of endothelial <i>Fundc1</i> in postnatal mice was sufficient to cause PH spontaneously, whereas augmenting endothelial <i>Fundc1</i> protected against PH before and after the onset of disease. Mechanistically, <i>Fundc1</i> deficiency impaired basal mitophagy in endothelial cells, leading to the accumulation of dysfunctional mitochondria, metabolic reprogramming toward aerobic glycolysis, pseudohypoxia, and senescence, likely via a mtROS-HIF2α signaling pathway. Subsequently, <i>Fundc1</i>-deficient endothelial cells increased IGFBP2 (insulin-like growth factor-binding protein 2) secretion that drove pulmonary arterial remodeling to instigate PH. Finally, proof-of-principle in vivo studies showed significant efficacy on PH amelioration by targeting endothelial mitophagy, pseudohypoxia, senescence, or IGFBP2.</p><p><strong>Conclusions: </strong>Collectively, we show that FUNDC1-mediated basal mitophagy is critical for endothelial homeostasis, and its disruption instigates PH pathogenesis. Given that similar changes in FUNDC1 and IGFBP2 were observed in PH patients, our findings are of significant clinical relevance and provide novel therapeutic strategies for PH.</p>","PeriodicalId":10147,"journal":{"name":"Circulation research","volume":" ","pages":""},"PeriodicalIF":16.5,"publicationDate":"2024-12-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142799625","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CAR-Macrophage Therapy Alleviates Myocardial Ischemia-Reperfusion Injury.","authors":"Jiawan Wang, Heng Du, Wanrun Xie, Jinmiao Bi, Hao Zhang, Xu Liu, Yuhan Wang, Shaolong Zhang, Anhua Lei, Chuting He, Hailong Yuan, Jiahe Zhang, Yujing Li, Pengfei Xu, Siqi Liu, Yanan Zhou, Jianghua Shen, Jingdong Wu, Yihong Cai, Chaofan Yang, Zeya Li, Yingxin Liang, Yang Zhao, Jin Zhang, Moshi Song","doi":"10.1161/CIRCRESAHA.124.325212","DOIUrl":"10.1161/CIRCRESAHA.124.325212","url":null,"abstract":"<p><strong>Background: </strong>Given the growing acknowledgment of the detrimental effects of excessive myocardial fibrosis on pathological remodeling after myocardial ischemia-reperfusion injury (I/R), targeting the modulation of myocardial fibrosis may offer protective and therapeutic advantages. However, effective clinical interventions and therapies that target myocardial fibrosis remain limited. As a promising chimeric antigen receptor (CAR) cell therapy, whether CAR macrophages (CAR-Ms) can be used to treat I/R remains unclear.</p><p><strong>Methods: </strong>The expression of FAP (fibroblast activation protein) was studied in mouse hearts after I/R. FAP CAR-Ms were generated to target FAP-expressing cardiac fibroblasts in mouse hearts after I/R. The phagocytosis activity of FAP CAR-Ms was tested in vitro. The efficacy and safety of FAP CAR-Ms in treating I/R were evaluated in vivo.</p><p><strong>Results: </strong>FAP was significantly upregulated in activated cardiac fibroblasts as early as 3 days after I/R. Upon demonstrating their ability to engulf FAP-overexpressing fibroblasts, we intravenously administered FAP CAR-Ms to mice at 3 days after I/R and found that FAP CAR-Ms significantly improved cardiac function and reduced myocardial fibrosis in mice after I/R. No toxicities associated with FAP CAR-Ms were detected in the heart or other organs at 2 weeks after I/R. Finally, we found that FAP CAR-Ms conferred long-term cardioprotection against I/R.</p><p><strong>Conclusions: </strong>Our proof-of-concept study demonstrates the therapeutic potential of FAP CAR-Ms in alleviating myocardial I/R and potentially opens new avenues for the treatment of a range of heart diseases that include a fibrotic phenotype.</p>","PeriodicalId":10147,"journal":{"name":"Circulation research","volume":" ","pages":"1161-1174"},"PeriodicalIF":16.5,"publicationDate":"2024-12-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142496114","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Kindlin-2 Phase Separation in Response to Flow Controls Vascular Stability.","authors":"Nina Ma, Fangfang Wu, Jiayu Liu, Ziru Wu, Lu Wang, Bochuan Li, Yuming Liu, Xue Dong, Junhao Hu, Xi Fang, Heng Zhang, Ding Ai, Jing Zhou, Xiaohong Wang","doi":"10.1161/CIRCRESAHA.124.324773","DOIUrl":"10.1161/CIRCRESAHA.124.324773","url":null,"abstract":"<p><strong>Background: </strong>Atheroprotective shear stress preserves endothelial barrier function, while atheroprone shear stress enhances endothelial permeability. Yet, the underlying mechanisms through which distinct flow patterns regulate EC integrity remain to be clarified. This study aimed to investigate the involvement of Kindlin-2, a key component of focal adhesion and endothelial adherens junctions crucial for regulating endothelial cell (EC) integrity and vascular stability.</p><p><strong>Methods: </strong>Mouse models of atherosclerosis in EC-specific <i>Kindlin-2</i> knockout mice (<i>Kindlin-2</i>^<i>iΔEC</i>) were used to study the role of Kindlin-2 in atherogenesis. Pulsatile shear (12±4 dynes/cm²) or oscillatory shear (0.5±4 dynes/cm²) were applied to culture ECs. Live-cell imaging, fluorescence recovery after photobleaching assay, and OptoDroplet assay were used to study the liquid-liquid phase separation (LLPS) of Kindlin-2. Co-immunoprecipitation, mutagenesis, proximity ligation assay, and transendothelial electrical resistance assay were used to explore the underlying mechanism of flow-regulated Kindlin-2 function.</p><p><strong>Results: </strong>We found that Kindlin-2 localization is altered under different flow patterns. <i>Kindlin-2</i>^<i>iΔEC</i> mice showed heightened vascular permeability. <i>Kindlin-2</i>^<i>iΔEC</i> were bred onto <i>ApoE</i>^<i>-/-</i> mice to generate <i>Kindlin-2</i>^<i>iΔEC</i>; <i>ApoE</i>^<i>-</i>^<i>/-</i> mice, which displayed a significant increase in atherosclerosis lesions. In vitro data showed that in ECs, Kindlin-2 underwent LLPS, a critical process for proper focal adhesion assembly, maturation, and junction formation. Mass spectrometry analysis revealed that oscillatory shear increased arginine methylation of Kindlin-2, catalyzed by PRMT5 (protein arginine methyltransferase 5). Functionally, arginine hypermethylation inhibits Kindlin-2 LLPS, impairing focal adhesion assembly and junction maturation. Notably, we identified R290 of Kindlin-2 as a crucial residue for LLPS and a key site for arginine methylation. Finally, pharmacologically inhibiting arginine methylation reduces EC activation and plaque formation.</p><p><strong>Conclusions: </strong>Collectively, our study elucidates that mechanical force induces arginine methylation of Kindlin-2, thereby regulating vascular stability through its impact on Kindlin-2 LLPS. Targeting Kindlin-2 arginine methylation emerges as a promising hemodynamic-based strategy for treating vascular disorders and atherosclerosis.</p>","PeriodicalId":10147,"journal":{"name":"Circulation research","volume":" ","pages":"1141-1160"},"PeriodicalIF":16.5,"publicationDate":"2024-12-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142567535","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Meet the First Authors.","authors":"","doi":"10.1161/RES.0000000000000704","DOIUrl":"https://doi.org/10.1161/RES.0000000000000704","url":null,"abstract":"","PeriodicalId":10147,"journal":{"name":"Circulation research","volume":"135 12","pages":"1120-1121"},"PeriodicalIF":16.5,"publicationDate":"2024-12-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142784296","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cytotoxic T Cells Drive Outcome in Inflammatory Dilated Cardiomyopathy.","authors":"Maurits A Sikking, Daniel Harding, Michiel T H M Henkens, Sophie L V M Stroeks, Max F G H M Venner, Bastien Nihant, Rick E W van Leeuwen, Silvia Fanti, Xiaofei Li, Pieter van Paassen, Christian Knackstedt, Hans-Peter Brunner-la Rocca, Vanessa P M van Empel, Job A J Verdonschot, Federica M Marelli-Berg, Stephane R B Heymans","doi":"10.1161/CIRCRESAHA.124.325183","DOIUrl":"10.1161/CIRCRESAHA.124.325183","url":null,"abstract":"","PeriodicalId":10147,"journal":{"name":"Circulation research","volume":" ","pages":"1193-1195"},"PeriodicalIF":16.5,"publicationDate":"2024-12-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11620291/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142459345","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"In This Issue.","authors":"","doi":"10.1161/RES.0000000000000703","DOIUrl":"https://doi.org/10.1161/RES.0000000000000703","url":null,"abstract":"","PeriodicalId":10147,"journal":{"name":"Circulation research","volume":"135 12","pages":"1119"},"PeriodicalIF":16.5,"publicationDate":"2024-12-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142784293","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}