Circulation最新文献

{"title":"Mitochondrial 1-Carbon Metabolism Drives CD34-Lineage Cells to Differentiate Into T Follicular Helper Cells to Form Tertiary Lymphoid Organs in Transplant Arteriosclerosis.","authors":"Xuejing Sun,Junru Wu,Tian He,Meng Yao,Li Qin,Chunyan Weng,Liping Peng,Qingzhong Xiao,Yao Lu,Hong Yuan,Qingbo Xu,Jingjing Cai","doi":"10.1161/circulationaha.125.073691","DOIUrl":"https://doi.org/10.1161/circulationaha.125.073691","url":null,"abstract":"BACKGROUNDAllograft arteriosclerosis, a significant cause of graft failure, is linked to the formation of tertiary lymphoid organs. T follicular helper (Tfh) cells are a vital subset of helper T cells that control the formation of the germinal center in tertiary lymphoid organs. Thus, understanding the origins and regulatory mechanisms of Tfh cells in allograft arteriosclerosis is essential for developing targeted therapies.METHODSWe used a lineage-tracing strategy to track Tfh cell fate in mouse models. Single-cell RNA sequencing, flow cytometry, and immunofluorescence staining were employed to analyze cell populations in remodeled arteries 2 and 4 weeks after transplantation. Additionally, we used VEGFR-3 inhibitors and lymph node dissection to suppress lymphatic vessel formation. Metabolic signatures and flux in different cell types were investigated using ultrahigh-performance liquid chromatography and high-resolution mass spectrometry-based metabolomics. CD4+ T cell-specific MTHFD2 knockout mice were used to corroborate our hypothesis about the role of mitochondrial 1-carbon metabolism in Tfh cell differentiation. Mechanisms discovered in vivo were also tested ex vivo.RESULTSCD34-lineage cells were found to be the major source of cells differentiating into T cell populations in allograft arteries. CD34-lineage cells mainly originated from the thymus, with drainage through lymphatic vessels, and differentiated into effective T cells around grafting arteries. Using CD34 lineage-tracing mice and single-cell RNA sequencing, we identified a Tfh cell population derived from CD34-lineage CD4+ T cells. Untargeted and targeted metabolomics revealed distinct upregulation of 1-carbon metabolism during CD4+ T-to-Tfh cell differentiation. Supplementation of amino acids essential for 1-carbon metabolism, such as serine, methionine or glycine, facilitated differentiation from CD4+ T to Tfh cells. Using deuterium-labeled serine, we found that the mitochondrial 1-carbon pathway is predominant. Inhibition of the mitochondrial 1-carbon metabolic enzyme MTHFD2 by administration of DS18561882 or generating CD4+ T cell-specific MTHFD2 knockout mice, significantly inhibited the numbers of Tfh cells and tertiary lymphoid organ formation as well as vascular remodeling.CONCLUSIONSThis study provides insights into the critical role of mitochondrial 1-carbon metabolism and MTHFD2 in governing the differentiation of CD34-lineage cells into Tfh cells, which contributes to tertiary lymphoid organ formation in transplant vasculopathy, offering potential therapeutic targets to enhance transplant outcomes.","PeriodicalId":10331,"journal":{"name":"Circulation","volume":"640 1","pages":""},"PeriodicalIF":37.8,"publicationDate":"2025-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144370205","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":"Letter by Wang et al Regarding Article, \"Bone Morphogenetic Protein 9 Protects Against Myocardial Infarction by Improving Lymphatic Drainage Function and Triggering DECR1-Mediated Mitochondrial Bioenergetics\".","authors":"Heng Wang,Taoran Zhao,Guoping Zheng","doi":"10.1161/circulationaha.124.072438","DOIUrl":"https://doi.org/10.1161/circulationaha.124.072438","url":null,"abstract":"","PeriodicalId":10331,"journal":{"name":"Circulation","volume":"242 1","pages":"e1091-e1092"},"PeriodicalIF":37.8,"publicationDate":"2025-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144370263","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":"Nonculprit Vulnerable Plaques and Prognosis in Myocardial Infarction With Versus Without ST-Segment Elevation: A PROSPECT II Substudy.","authors":"Pernille G Thrane,Michael Maeng,Akiko Maehara,Hans Erik Bøtker,Gary S Mintz,Lars Kjøller-Hansen,Thomas Engstrøm,Mitsuaki Matsumura,Lak N Kotinkaduwa,Ole Fröbert,Jonas Persson,Rune Wiseth,Alf I Larsen,Lisette O Jensen,Jan E Nordrehaug,Øyvind Bleie,Claes Held,Stefan K James,Ziad A Ali,David Erlinge,Gregg W Stone","doi":"10.1161/circulationaha.124.071980","DOIUrl":"https://doi.org/10.1161/circulationaha.124.071980","url":null,"abstract":"BACKGROUNDClinical guidelines recommend different revascularization strategies for nonculprit lesions in patients with ST-segment-elevation myocardial infarction (STEMI) versus non-STEMI (NSTEMI). Whether the prevalence of untreated high-risk vulnerable plaques differs in STEMI and NSTEMI and affects their outcomes is unknown.METHODSIn PROSPECT II (Providing Regional Observations to Study Predictors of Events in the Coronary Tree II), a multicenter, prospective natural history study, patients with recent myocardial infarction underwent 3-vessel coronary angiography with coregistered near-infrared spectroscopy and intravascular ultrasound after successful percutaneous coronary intervention of obstructive lesions from 2014 through 2017. Two-feature high-risk plaques were defined as those with both plaque burden ≥70% and maximum lipid core burden index over any 4-mm segment ≥324.7. The primary end point was major adverse cardiovascular events arising from untreated nonculprit lesions during a median 3.7-year follow-up.RESULTSOf 898 patients, 199 (22.2%) with 849 nonculprit lesions had STEMI and 699 (77.8%) with 2784 nonculprit lesions had NSTEMI. By intravascular ultrasound, the median nonculprit lesion length was 17.4 mm (interquartile range, 16.3-18.5) in STEMI and 17.7 mm (interquartile range, 17.1-18.4) in NSTEMI (P=0.63), and the median minimal lumen area was 5.5 mm2 (interquartile range, 5.3-5.7 mm2) in STEMI and 5.5 mm2 (interquartile range, 5.3-5.6 mm2) in NSTEMI (P=0.99). At the lesion level, the prevalence of 2-feature high-risk nonobstructive nonculprit plaques was slightly higher in patients with STEMI than in patients with NSTEMI (12.8% versus 10.1%; P=0.03). At the patient level, however, the prevalence of 2-feature high-risk plaques was similar in STEMI versus NSTEMI (38.8% versus 32.7%; P=0.11). The prevalence of patients with 1 or more lesions meeting at least 1 high-risk plaque criterion was also similar (plaque burden ≥70%, 63.3% versus 57.8% [P=0.16]; maximum lipid core burden index over any 4-mm segment ≥324.7, 63.3% versus 57.6% [P=0.15]). The 4-year rates of nonculprit lesion-related major adverse cardiovascular events were similar in STEMI versus NSTEMI (8.6% versus 7.8%; hazard ratio, 1.02 [95% CI, 0.57-1.81]; P=0.95), as were the rates of all major adverse cardiovascular events (14.2% versus 13.0%; hazard ratio, 1.06 [95% CI, 0.68-1.64]; P=0.80).CONCLUSIONSIn the PROSPECT II study, the per-patient prevalence of high-risk vulnerable plaques was comparable in STEMI versus NSTEMI, as was the overall long-term incidence of nonculprit lesion-related and all major adverse cardiovascular events. These results support a similar revascularization strategy for nonculprit lesions in patients with STEMI or NSTEMI after culprit lesion management.REGISTRATIONURL: https://www.clinicaltrials.gov; Unique identifier: NCT02171065.","PeriodicalId":10331,"journal":{"name":"Circulation","volume":"25 1","pages":"1767-1779"},"PeriodicalIF":37.8,"publicationDate":"2025-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144370264","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":"Insights Into Recovery From Acute Fulminant Myocarditis Following Successful Treatment With Ruxolitinib by Comprehensive Single-Cell Profiling.","authors":"Juan Qin,Mandar A Aras,Evelyn J Song,Andrew J Connolly,Lylybell Zhou,Connor O'Brien,Joe-Elie Salem,Arun Padmanabhan,Javid J Moslehi","doi":"10.1161/circulationaha.124.073058","DOIUrl":"https://doi.org/10.1161/circulationaha.124.073058","url":null,"abstract":"","PeriodicalId":10331,"journal":{"name":"Circulation","volume":"19 1","pages":"1814-1817"},"PeriodicalIF":37.8,"publicationDate":"2025-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144370260","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":"Correction to: 2025 Heart Disease and Stroke Statistics: A Report of US and Global Data From the American Heart Association.","authors":"Seth S Martin,Aaron W Aday,Norrina B Allen,Zaid I Almarzooq,Cheryl A M Anderson,Pankaj Arora,Christy L Avery,Carissa M Baker-Smith,Nisha Bansal,Andrea Z Beaton,Yvonne Commodore-Mensah,Maria E Currie,Mitchell S V Elkind,Wenjun Fan,Giuliano Generoso,Bethany Barone Gibbs,Debra G Heard,Swapnil Hiremath,Michelle C Johansen,Dhruv S Kazi,Darae Ko,Michelle H Leppert,Jared W Magnani,Erin D Michos,Michael E Mussolino,Nisha I Parikh,Sarah M Perman,Mary Rezk-Hanna,Gregory A Roth,Nilay S Shah,Mellanie V Springer,Marie-Pierre St-Onge,Evan L Thacker,Sarah M Urbut,Harriette G C Van Spall,Jenifer H Voeks,Seamus P Whelton,Nathan D Wong,Sally S Wong,Kristine Yaffe,Latha P Palaniappan,","doi":"10.1161/cir.0000000000001345","DOIUrl":"https://doi.org/10.1161/cir.0000000000001345","url":null,"abstract":"","PeriodicalId":10331,"journal":{"name":"Circulation","volume":"269 1","pages":"e1096"},"PeriodicalIF":37.8,"publicationDate":"2025-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144370257","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":"Response by Duan and Lin to Letter Regarding Article, \"Bone Morphogenetic Protein 9 Protects Against Myocardial Infarction by Improving Lymphatic Drainage Function and Triggering DECR1-Mediated Mitochondrial Bioenergetics\".","authors":"Zikun Duan,Zhuofeng Lin","doi":"10.1161/circulationaha.125.074590","DOIUrl":"https://doi.org/10.1161/circulationaha.125.074590","url":null,"abstract":"","PeriodicalId":10331,"journal":{"name":"Circulation","volume":"45 1","pages":"e1093-e1094"},"PeriodicalIF":37.8,"publicationDate":"2025-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144370262","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":"Abelacimab Versus Rivaroxaban in Patients With Atrial Fibrillation on Antiplatelet Therapy: A Prespecified Analysis of the AZALEA-TIMI 71 Trial.","authors":"Samer Al Said, Siddharth M Patel, Robert P Giugliano, David A Morrow, Erica L Goodrich, Sabina A Murphy, Bruce Hug, Sanobar Parkar, Shih-Ann Chen, Shaun G Goodman, Boyoung Joung, Robert G Kiss, Wojciech Wojakowski, Jeffrey I Weitz, Dan Bloomfield, Marc S Sabatine, Christian T Ruff","doi":"10.1161/CIRCULATIONAHA.125.074037","DOIUrl":"https://doi.org/10.1161/CIRCULATIONAHA.125.074037","url":null,"abstract":"<p><strong>Background: </strong>Combining antiplatelet therapy (APT) with conventional anticoagulants increases the risk of bleeding. In the AZALEA-TIMI 71 trial (Safety and Tolerability of Abelacimab [MAA868] vs Rivaroxaban in Patients With Atrial Fibrillation), the novel factor XI inhibitor abelacimab significantly reduced the risk of bleeding compared with rivaroxaban in patients with atrial fibrillation. Whether the safety of combination antithrombotic therapy differs in the context of factor XI inhibition has not been well characterized.</p><p><strong>Methods: </strong>This prespecified analysis of AZALEA-TIMI 71 includes patients randomized between March and December of 2021 to 1 of 2 subcutaneous monthly abelacimab doses (90 or 150 mg) or oral rivaroxaban (20 mg daily, dose reduced to 15 mg in patients with creatinine clearance ≤50 mL/min), stratified by planned use of concomitant APT. The primary composite of major or clinically relevant nonmajor bleeding and other safety and efficacy outcomes were examined by concomitant APT and randomized treatment.</p><p><strong>Results: </strong>Of 1287 patients (44% female; median age, 74 years [interquartile range, 69-78]), 318 (24.7%) were on APT at baseline with planned continuation (15.5% aspirin only, 7.5% P2Y<sub>12</sub> inhibitor only, and 1.6% dual APT). In the rivaroxaban arm, the rate of major or clinically relevant nonmajor bleeding was 10.6% per 100 patient-years with concomitant APT versus 7.7% per 100 patient-years without. In the abelacimab arms, the rates were 2.5% and 3.5% per 100 patient-years for the 90-mg and 150-mg doses, respectively, with concomitant APT and 2.7% and 3.1% per 100 patient-years without. Each abelacimab dose significantly reduced major or clinically relevant nonmajor bleeding compared with rivaroxaban, both in those with concomitant APT (adjusted hazard ratio, 0.26 [95% CI, 0.10-0.70] and hazard ratio, 0.30 [95% CI, 0.12-0.74] for 90 mg and 150 mg of abelacimab, respectively, versus rivaroxaban) and in those without concomitant APT (adjusted hazard ratio, 0.34 [95% CI, 0.19-0.60] and hazard ratio, 0.40 [95% CI, 0.23-0.68] for 90 mg and 150 mg of abelacimab, respectively; <i>P</i><sub>interactions</sub>=0.56 and 0.60, respectively). Patients with concomitant APT tended to derive greater absolute risk reductions with abelacimab (8.1% and 7.1% for 90 mg and 150 mg of abelacimab, respectively, versus rivaroxaban) than those without concomitant APT (5.0% and 4.6%, respectively).</p><p><strong>Conclusions: </strong>Inhibition of factor XI with abelacimab consistently reduced bleeding compared with rivaroxaban regardless of concomitant APT use, with greater absolute reductions in bleeding in those requiring concomitant APT. These data suggest that factor XI inhibition may be a safe anticoagulant option in patients with atrial fibrillation requiring concomitant APT.</p><p><strong>Registration: </strong>URL: https://www.clinicaltrials.gov; Unique identifier: NCT04755283.","PeriodicalId":10331,"journal":{"name":"Circulation","volume":" ","pages":""},"PeriodicalIF":35.5,"publicationDate":"2025-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144367948","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":"Confounders, Effect Modifiers, and Mediators: Dealing With \"Third Variables\" in Cardiovascular Epidemiology.","authors":"Andrea Bellavia,Sabina A Murphy","doi":"10.1161/circulationaha.125.073645","DOIUrl":"https://doi.org/10.1161/circulationaha.125.073645","url":null,"abstract":"","PeriodicalId":10331,"journal":{"name":"Circulation","volume":"54 1","pages":"1755-1757"},"PeriodicalIF":37.8,"publicationDate":"2025-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144370266","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":"A Systematic Review of \"Food Is Medicine\" Randomized Controlled Trials for Noncommunicable Disease in the United States: A Scientific Statement From the American Heart Association.","authors":"Hilary K Seligman,Sonia Y Angell,Seth A Berkowitz,Mitchell S V Elkind,Kurt Hager,Nathalie Moise,Hannah Posner,Jen Muse,Angela Odoms-Young,Ronit Ridberg,Andrea B Troxel,Amy L Yaroch,Kevin G Volpp","doi":"10.1161/cir.0000000000001343","DOIUrl":"https://doi.org/10.1161/cir.0000000000001343","url":null,"abstract":"Poor diet quality is a leading risk factor for cardiometabolic disease (ie, diabetes and diseases associated with metabolism and inflammation), which is present in about half of American adults. Support has grown for incorporating the provision of healthy food as a complement to or a component of clinical care. Such \"Food Is Medicine\" programs provide free or subsidized healthy food directly to patients in close coordination with the health care system. In this review, we systematically examined published randomized controlled trials examining Food Is Medicine programs in the United States, categorizing them into different stages of development using the National Institutes of Health Model for Behavioral Intervention Development. This review identified a total of 14 randomized controlled trials of Food Is Medicine interventions in the United States with noncommunicable disease outcomes, more than one-third of which were early-stage smaller-scale trials (stage 1 randomized controlled trials). Broad variations in populations enrolled; intervention design, duration, and intensity; and outcomes precluded many direct comparisons between studies. Randomized controlled trial data were generally consistent with findings in the observational literature, indicating that common Food Is Medicine approaches often positively influence diet quality and food security, which are theorized to be key mediators for clinical outcomes. However, the impact on clinical outcomes was inconsistent and often failed to reach statistical significance. These observations highlight the need for larger, higher-quality Food Is Medicine studies focusing on the measurement of clinical outcomes within well-designed programs and the need for additional randomized controlled trials that more systematically map out the relationship between participation in different types of Food Is Medicine programs and health outcomes.","PeriodicalId":10331,"journal":{"name":"Circulation","volume":"39 1","pages":""},"PeriodicalIF":37.8,"publicationDate":"2025-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144311327","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":"Splenic CD169⁺Tim4⁺ Marginal Metallophilic Macrophages Are Essential for Wound Healing After Myocardial Infarction.","authors":"Mohamed Ameen Ismahil, Guihua Zhou, Shreya Rajasekar, Min Gao, Shyam S Bansal, Bindiya Patel, Nita Limdi, Min Xie, Sergey Antipenko, Gregg Rokosh, Tariq Hamid, Sumanth D Prabhu","doi":"10.1161/CIRCULATIONAHA.124.071772","DOIUrl":"10.1161/CIRCULATIONAHA.124.071772","url":null,"abstract":"<p><strong>Background: </strong>Fidelity of wound healing after myocardial infarction (MI) is an important determinant of subsequent adverse cardiac remodeling and failure. Macrophages derived from infiltrating Ly6C^hi (lymphocyte antigen 6 complex, locus C) blood monocytes are a key component of this healing response; however, the importance of other macrophage populations is unclear.</p><p><strong>Methods: </strong>We used a variety of in vivo murine models and orthogonal approaches, including surgical MI, flow cytometry and single-cell RNA sequencing, lineage tracing and cell tracking, splenectomy, parabiosis, cell adoptive transfer, and functional characterization, to establish an essential role for splenic CD169⁺Tim4⁺ (cluster of differentiation 169⁺; T cell immunoglobulin- and mucin-domain-containing molecule 4) marginal metallophilic macrophages (MMMs) in post-MI wound healing in mice. Flow cytometry was used to measure circulating CD169⁺Tim4⁺ monocytes in humans with ST-segment-elevation MI and control participants with stable coronary artery disease undergoing elective percutaneous coronary intervention.</p><p><strong>Results: </strong>Splenic CD169⁺Tim4⁺ MMMs circulate in blood as Ly6C^low monocytes expressing macrophage markers and help populate CD169⁺Tim4⁺CCR2^-LYVE1^low macrophages in the naive heart. After acute MI, splenic MMMs augment phagocytosis and CCR (C-C motif chemokine receptor) 3 and CCR4 expression, and robustly mobilize to the heart, resulting in marked expansion of cardiac CD169⁺Tim4⁺LYVE1^low macrophages with an immunomodulatory and proresolving gene signature. These macrophages are obligatory for apoptotic neutrophil clearance, suppression of inflammation, and induction of a reparative macrophage phenotype in the infarcted heart. Splenic MMMs are both necessary and sufficient for post-MI wound healing, and limit late pathological remodeling. Liver X receptor-α agonist-induced expansion of the splenic marginal zone and MMMs during acute MI alleviates inflammation and improves short- and long-term cardiac remodeling. Humans with acute ST-segment-elevation MI also exhibit expansion of circulating CD169⁺Tim4⁺ cells, primarily within the intermediate (CD14⁺CD16⁺) monocyte population.</p><p><strong>Conclusions: </strong>Splenic CD169⁺Tim4⁺ MMMs are required for proresolving and reparative responses after MI and can be manipulated for therapeutic benefit to limit long-term heart failure.</p>","PeriodicalId":10331,"journal":{"name":"Circulation","volume":" ","pages":"1712-1729"},"PeriodicalIF":35.5,"publicationDate":"2025-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12165546/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143984044","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}