Circulation research最新文献

{"title":"SGLT2 Inhibitors Act Independently of SGLT2 to Confer Benefit for HFrEF in Mice.","authors":"Justin H Berger, Timothy R Matsuura, Caitlyn E Bowman, Renee Taing, Jiten Patel, Ling Lai, Teresa C Leone, Jeffrey D Reagan, Saptarsi M Haldar, Zoltan Arany, Daniel P Kelly","doi":"10.1161/CIRCRESAHA.124.324823","DOIUrl":"10.1161/CIRCRESAHA.124.324823","url":null,"abstract":"","PeriodicalId":10147,"journal":{"name":"Circulation research","volume":" ","pages":"632-634"},"PeriodicalIF":16.5,"publicationDate":"2024-08-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11326968/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141747479","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":"Lysozyme 1 Inflamed CCR2⁺ Macrophages Promote Obesity-Induced Cardiac Dysfunction.","authors":"Lai Zhang, Huian Han, Andi Xu, Adwait Sathe, Siying Fu, Jiaqi Zhao, Wenhan Cai, Yaqing Yang, Jinting Liu, Hui Bai, Jingjing Ben, Xudong Zhu, Xiaoyu Li, Qing Yang, Zidun Wang, Yayun Gu, Chao Xing, Gabriele G Schiattarella, Steven Yan Cheng, Hanwen Zhang, Qi Chen","doi":"10.1161/CIRCRESAHA.124.324106","DOIUrl":"10.1161/CIRCRESAHA.124.324106","url":null,"abstract":"<p><strong>Background: </strong>Macrophages are key players in obesity-associated cardiovascular diseases, which are marked by inflammatory and immune alterations. However, the pathophysiological mechanisms underlying macrophage's role in obesity-induced cardiac inflammation are incompletely understood. Our study aimed to identify the key macrophage population involved in obesity-induced cardiac dysfunction and investigate the molecular mechanism that contributes to the inflammatory response.</p><p><strong>Methods: </strong>In this study, we used single-cell RNA-sequencing analysis of Cd45⁺CD11b⁺F4/80⁺ cardiac macrophages to explore the heterogeneity of cardiac macrophages. The CCR2⁺ (C-C chemokine receptor 2) macrophages were specifically removed by a dual recombinase approach, and the macrophage CCR2 was deleted to investigate their functions. We also performed cleavage under target and tagmentation analysis, chromatin immunoprecipitation-polymerase chain reaction, luciferase assay, and macrophage-specific lentivirus transfection to define the impact of lysozyme C in macrophages on obesity-induced inflammation.</p><p><strong>Results: </strong>We find that the <i>Ccr2</i> cluster undergoes a functional transition from homeostatic maintenance to proinflammation. Our data highlight specific changes in macrophage behavior during cardiac dysfunction under metabolic challenge. Consistently, inducible ablation of CCR2⁺CX3CR1⁺ macrophages or selective deletion of macrophage CCR2 prevents obesity-induced cardiac dysfunction. At the mechanistic level, we demonstrate that the obesity-induced functional shift of CCR2-expressing macrophages is mediated by the CCR2/activating transcription factor 3/lysozyme 1/NF-κB (nuclear factor kappa B) signaling. Finally, we uncover a noncanonical role for lysozyme 1 as a transcription activator, binding to the <i>RelA</i> promoter, driving NF-κB signaling, and strongly promoting inflammation and cardiac dysfunction in obesity.</p><p><strong>Conclusions: </strong>Our findings suggest that lysozyme 1 may represent a potential target for the diagnosis of obesity-induced inflammation and the treatment of obesity-induced heart disease.</p>","PeriodicalId":10147,"journal":{"name":"Circulation research","volume":" ","pages":"596-613"},"PeriodicalIF":16.5,"publicationDate":"2024-08-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141757433","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.0000000000000687","DOIUrl":"https://doi.org/10.1161/RES.0000000000000687","url":null,"abstract":"","PeriodicalId":10147,"journal":{"name":"Circulation research","volume":"135 5","pages":"552-553"},"PeriodicalIF":16.5,"publicationDate":"2024-08-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141987529","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.0000000000000687","DOIUrl":"https://doi.org/10.1161/RES.0000000000000687","url":null,"abstract":"","PeriodicalId":10147,"journal":{"name":"Circulation research","volume":"135 5","pages":"552-553"},"PeriodicalIF":16.5,"publicationDate":"2024-08-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142035420","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":"Variables Predicting Experimental Stroke Outcome: How Well Do We Know Our Models?","authors":"Matthias Endres, Nikolaus Plesnila, Johannes Boltze","doi":"10.1161/CIRCRESAHA.124.325129","DOIUrl":"https://doi.org/10.1161/CIRCRESAHA.124.325129","url":null,"abstract":"","PeriodicalId":10147,"journal":{"name":"Circulation research","volume":"135 5","pages":"593-595"},"PeriodicalIF":16.5,"publicationDate":"2024-08-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141987531","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":"Dysferlin Enables Tubular Membrane Proliferation in Cardiac Hypertrophy.","authors":"Nora Josefine Paulke, Carolin Fleischhacker, Justus B Wegener, Gabriel C Riedemann, Constantin Cretu, Mufassra Mushtaq, Nina Zaremba, Wiebke Möbius, Yannik Zühlke, Jasper Wedemeyer, Lorenz Liebmann, Anastasiia A Gorshkova, Daniel Kownatzki-Danger, Eva Wagner, Tobias Kohl, Carolin Wichmann, Olaf Jahn, Henning Urlaub, Karl Toischer, Gerd Hasenfuß, Tobias Moser, Julia Preobraschenski, Christof Lenz, Eva A Rog-Zielinska, Stephan E Lehnart, Sören Brandenburg","doi":"10.1161/CIRCRESAHA.124.324588","DOIUrl":"10.1161/CIRCRESAHA.124.324588","url":null,"abstract":"<p><strong>Background: </strong>Cardiac hypertrophy compensates for increased biomechanical stress of the heart induced by prevalent cardiovascular pathologies but can result in heart failure if left untreated. Here, we hypothesized that the membrane fusion and repair protein dysferlin is critical for the integrity of the transverse-axial tubule (TAT) network inside cardiomyocytes and contributes to the proliferation of TAT endomembranes during pressure overload-induced cardiac hypertrophy.</p><p><strong>Methods: </strong>Stimulated emission depletion and electron microscopy were used to localize dysferlin in mouse and human cardiomyocytes. Data-independent acquisition mass spectrometry revealed the cardiac dysferlin interactome and proteomic changes of the heart in dysferlin-knockout mice. After transverse aortic constriction, we compared the hypertrophic response of wild-type versus dysferlin-knockout hearts and studied TAT network remodeling mechanisms inside cardiomyocytes by live-cell membrane imaging.</p><p><strong>Results: </strong>We localized dysferlin in a vesicular compartment in nanometric proximity to contact sites of the TAT network with the sarcoplasmic reticulum, a.k.a. junctional complexes for Ca²⁺-induced Ca²⁺ release. Interactome analyses demonstrated a novel protein interaction of dysferlin with the membrane-tethering sarcoplasmic reticulum protein juncophilin-2, a putative interactor of L-type Ca²⁺ channels and ryanodine receptor Ca²⁺ release channels in junctional complexes. Although the dysferlin-knockout caused a mild progressive phenotype of dilated cardiomyopathy, global proteome analysis revealed changes preceding systolic failure. Following transverse aortic constriction, dysferlin protein expression was significantly increased in hypertrophied wild-type myocardium, while dysferlin-knockout animals presented markedly reduced left-ventricular hypertrophy. Live-cell membrane imaging showed a profound reorganization of the TAT network in wild-type left-ventricular myocytes after transverse aortic constriction with robust proliferation of axial tubules, which critically depended on the increased expression of dysferlin within newly emerging tubule components.</p><p><strong>Conclusions: </strong>Dysferlin represents a new molecular target in cardiac disease that protects the integrity of tubule-sarcoplasmic reticulum junctional complexes for regulated excitation-contraction coupling and controls TAT network reorganization and tubular membrane proliferation in cardiomyocyte hypertrophy induced by pressure overload.</p>","PeriodicalId":10147,"journal":{"name":"Circulation research","volume":" ","pages":"554-574"},"PeriodicalIF":16.5,"publicationDate":"2024-08-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141619462","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":"mTORC1 Signaling in Brain Endothelial Progenitors Contributes to CCM Pathogenesis.","authors":"Wang Min, Lingfeng Qin, Haifeng Zhang, Francesc López-Giráldez, Ning Jiang, Yeaji Kim, Varsha K Mohan, Minhong Su, Katie N Murray, Jaime Grutzendler, Jenny Huanjiao Zhou","doi":"10.1161/CIRCRESAHA.123.324015","DOIUrl":"10.1161/CIRCRESAHA.123.324015","url":null,"abstract":"<p><strong>Background: </strong>Cerebral vascular malformations (CCMs) are primarily found within the brain, where they result in increased risk for stroke, seizures, and focal neurological deficits. The unique feature of the brain vasculature is the blood-brain barrier formed by the brain neurovascular unit. Recent studies suggest that loss of CCM genes causes disruptions of blood-brain barrier integrity as the inciting events for CCM development. CCM lesions are proposed to be initially derived from a single clonal expansion of a subset of angiogenic venous capillary endothelial cells (ECs) and respective resident endothelial progenitor cells (EPCs). However, the critical signaling events in the subclass of brain ECs/EPCs for CCM lesion initiation and progression are unclear.</p><p><strong>Methods: </strong>Brain EC-specific CCM3-deficient (<i>Pdcd10</i>^BECKO) mice were generated by crossing <i>Pdcd10</i>^<i>fl/fl</i> mice with <i>Mfsd2a</i>-CreER^T2 mice. Single-cell RNA-sequencing analyses were performed by the chromium single-cell platform (10× genomics). Cell clusters were annotated into EC subtypes based on visual inspection and GO analyses. Cerebral vessels were visualized by 2-photon in vivo imaging and tissue immunofluorescence analyses. Regulation of mTOR (mechanistic target of rapamycin) signaling by CCM3 and Cav1 (caveolin-1) was performed by cell biology and biochemical approaches.</p><p><strong>Results: </strong>Single-cell RNA-sequencing analyses from P10 <i>Pdcd1</i>0^BECKO mice harboring visible CCM lesions identified upregulated CCM lesion signature and mitotic EC clusters but decreased blood-brain barrier-associated EC clusters. However, a unique EPC cluster with high expression levels of stem cell markers enriched with mTOR signaling was identified from early stages of the P6 <i>Pdcd1</i>0^BECKO brain. Indeed, mTOR signaling was upregulated in both mouse and human CCM lesions. Genetic deficiency of Raptor (regulatory-associated protein of mTOR), but not of Rictor (rapamycin-insensitive companion of mTOR), prevented CCM lesion formation in the <i>Pdcd10</i>^BECKO model. Importantly, the mTORC1 (mTOR complex 1) pharmacological inhibitor rapamycin suppressed EPC proliferation and ameliorated CCM pathogenesis in <i>Pdcd10</i>^BECKO mice. Mechanistic studies suggested that Cav1/caveolae increased in CCM3-depleted EPC-mediated intracellular trafficking and complex formation of the mTORC1 signaling proteins.</p><p><strong>Conclusions: </strong>CCM3 is critical for maintaining blood-brain barrier integrity and CCM3 loss-induced mTORC1 signaling in brain EPCs initiates and facilitates CCM pathogenesis.</p>","PeriodicalId":10147,"journal":{"name":"Circulation research","volume":" ","pages":"e94-e113"},"PeriodicalIF":16.5,"publicationDate":"2024-08-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11293987/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141491102","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":"Imaging of Existing and Newly Translated Proteins Elucidates Mechanisms of Sarcomere Turnover.","authors":"Guy Douvdevany, Itai Erlich, Lilac Haimovich-Caspi, Tomer Mashiah, Maksymilian Prondzynski, Maria Rosaria Pricolo, Jorge Alegre-Cebollada, Wolfgang A Linke, Lucie Carrier, Izhak Kehat","doi":"10.1161/CIRCRESAHA.123.323819","DOIUrl":"10.1161/CIRCRESAHA.123.323819","url":null,"abstract":"<p><strong>Background: </strong>How the sarcomeric complex is continuously turned over in long-living cardiomyocytes is unclear. According to the prevailing model of sarcomere maintenance, sarcomeres are maintained by cytoplasmic soluble protein pools with free recycling between pools and sarcomeres.</p><p><strong>Methods: </strong>We imaged and quantified the turnover of expressed and endogenous sarcomeric proteins, including the giant protein titin, in cardiomyocytes in culture and in vivo, at the single cell and at the single sarcomere level using pulse-chase labeling of Halo-tagged proteins with covalent ligands.</p><p><strong>Results: </strong>We disprove the prevailing protein pool model and instead show an ordered mechanism in which only newly translated proteins enter the sarcomeric complex while older ones are removed and degraded. We also show that degradation is independent of protein age and that proteolytic extraction is a rate-limiting step in the turnover. We show that replacement of sarcomeric proteins occurs at a similar rate within cells and across the heart and is slower in adult cells.</p><p><strong>Conclusions: </strong>Our findings establish a unidirectional replacement model for cardiac sarcomeres subunit replacement and identify their turnover principles.</p>","PeriodicalId":10147,"journal":{"name":"Circulation research","volume":" ","pages":"474-487"},"PeriodicalIF":16.5,"publicationDate":"2024-08-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141497267","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":"L-Wnk1 Deletion in Smooth Muscle Cells Causes Aortitis and Inflammatory Shift.","authors":"Helene Quelquejay, Rida Al-Rifai, Michele Silvestro, Marie Vandestienne, Irmine Ferreira, Tristan Mirault, Daniel Henrion, Xiaodan Zhong, Icia Santos-Zas, Guillaume Goudot, Paul Alayrac, Estelle Robidel, Gwennhael Autret, Daniel Balvay, Soraya Taleb, Alain Tedgui, Chantal M Boulanger, Alma Zernecke, Antoine-Emmanuel Saliba, Juliette Hadchouel, Bhama Ramkhelawon, Clement Cochain, Sonia Bergaya, Xavier Jeunemaitre, Hafid Ait-Oufella","doi":"10.1161/CIRCRESAHA.124.324366","DOIUrl":"10.1161/CIRCRESAHA.124.324366","url":null,"abstract":"<p><strong>Background: </strong>The long isoform of the Wnk1 (with-no-lysine [K] kinase 1) is a ubiquitous serine/threonine kinase, but its role in vascular smooth muscle cells (VSMCs) pathophysiology remains unknown.</p><p><strong>Methods: </strong>AngII (angiotensin II) was infused in <i>Apoe^-/-</i> to induce experimental aortic aneurysm. Mice carrying an <i>Sm22-Cre</i> allele were cross-bred with mice carrying a floxed <i>Wnk1</i> allele to specifically investigate the functional role of Wnk1 in VSMCs.</p><p><strong>Results: </strong>Single-cell RNA-sequencing of the aneurysmal abdominal aorta from AngII-infused <i>Apoe^-/-</i> mice revealed that VSMCs that did not express Wnk1 showed lower expression of contractile phenotype markers and increased inflammatory activity. Interestingly, WNK1 gene expression in VSMCs was decreased in human abdominal aortic aneurysm. <i>Wnk1</i>-deficient VSMCs lost their contractile function and exhibited a proinflammatory phenotype, characterized by the production of matrix metalloproteases, as well as cytokines and chemokines, which contributed to local accumulation of inflammatory macrophages, Ly6C^hi monocytes, and γδ T cells. <i>Sm22Cre+Wnk1</i>^{<i>lox/lox</i>} mice spontaneously developed aortitis in the infrarenal abdominal aorta, which extended to the thoracic area over time without any negative effect on long-term survival. AngII infusion in <i>Sm22Cre+Wnk1</i>^{<i>lox/lox</i>} mice aggravated the aortic disease, with the formation of lethal abdominal aortic aneurysms. Pharmacological blockade of γδ T-cell recruitment using neutralizing anti-CXCL9 (anti-CXC motif chemokine ligand 9) antibody treatment, or of monocyte/macrophage using Ki20227, a selective inhibitor of CSF1 receptor, attenuated aortitis. <i>Wnk1</i> deletion in VSMCs led to aortic wall remodeling with destruction of elastin layers, increased collagen content, and enhanced local TGF-β (transforming growth factor-beta) 1 expression. Finally, in vivo TGF-β blockade using neutralizing anti-TGF-β antibody promoted saccular aneurysm formation and aorta rupture in <i>Sm22 Cre+ Wnk1</i>^{<i>lox/lox</i>} mice but not in control animals.</p><p><strong>Conclusion: </strong>Wnk1 is a key regulator of VSMC function. <i>Wnk1</i> deletion promotes VSMC phenotype switch toward a pathogenic proinflammatory phenotype, orchestrating deleterious vascular remodeling and spontaneous severe aortitis in mice.</p>","PeriodicalId":10147,"journal":{"name":"Circulation research","volume":" ","pages":"488-502"},"PeriodicalIF":16.5,"publicationDate":"2024-08-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141558190","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":"RNF149 Destabilizes IFNGR1 in Macrophages to Favor Postinfarction Cardiac Repair.","authors":"Chun-Kai Huang, Zhiyong Chen, Zhongxing Zhou, Shuaijie Chen, Longqing Chen, Liliang Li, Tao Li, Xiaoxiang Yan, Dajun Chai","doi":"10.1161/CIRCRESAHA.123.324023","DOIUrl":"10.1161/CIRCRESAHA.123.324023","url":null,"abstract":"<p><strong>Background: </strong>Macrophage-driven inflammation critically involves in cardiac injury and repair following myocardial infarction (MI). However, the intrinsic mechanisms that halt the immune response of macrophages, which is critical to preserve homeostasis and effective infarct repair, remain to be fully defined. Here, we aimed to determine the ubiquitination-mediated regulatory effects on averting exaggerated inflammatory responses in cardiac macrophages.</p><p><strong>Methods: </strong>We used transcriptome analysis of mouse cardiac macrophages and bone marrow-derived macrophages to identify the E3 ubiquitin ligase RNF149 (ring finger protein 149) as a modulator of macrophage response to MI. Employing loss-of-function methodologies, bone marrow transplantation approaches, and adenovirus-mediated RNF149 overexpression in macrophages, we elucidated the functional role of RNF149 in MI. We explored the underlying mechanisms through flow cytometry, transcriptome analysis, immunoprecipitation/mass spectrometry analysis, and functional experiments. RNF149 expression was measured in the cardiac tissues of patients with acute MI and healthy controls.</p><p><strong>Results: </strong>RNF149 was highly expressed in murine and human cardiac macrophages at the early phase of MI. Knockout of RNF149, transplantation of <i>Rnf149</i>^-/- bone marrow, and bone marrow macrophage-specific RNF149-knockdown markedly exacerbated cardiac dysfunction in murine MI models. Conversely, overexpression of RNF149 in macrophages attenuated the ischemia-induced decline in cardiac contractile function. RNF149 deletion increased infiltration of proinflammatory monocytes/macrophages, accompanied by a hastened decline in reparative subsets, leading to aggravation of myocardial apoptosis and impairment of infarct healing. Our data revealed that RNF149 in infiltrated macrophages restricted inflammation by promoting ubiquitylation-dependent proteasomal degradation of IFNGR1 (interferon gamma receptor 1). Loss of IFNGR1 rescued deleterious effects of RNF149 deficiency on MI. We further demonstrated that STAT1 (signal transducer and activator of transcription 1) activation induced <i>Rnf149</i> transcription, which, in turn, destabilized the IFNGR1 protein to counteract type-II IFN (interferon) signaling, creating a feedback control mechanism to fine-tune macrophage-driven inflammation.</p><p><strong>Conclusions: </strong>These findings highlight the significance of RNF149 as a molecular brake on macrophage response to MI and uncover a macrophage-intrinsic posttranslational mechanism essential for maintaining immune homeostasis and facilitating cardiac repair following MI.</p>","PeriodicalId":10147,"journal":{"name":"Circulation research","volume":" ","pages":"518-536"},"PeriodicalIF":16.5,"publicationDate":"2024-08-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141579122","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}