Pub Date : 2025-11-07DOI: 10.1038/s44161-025-00750-x
Andrea Tavosanis
{"title":"Bone marrow inflammation leads to hematotoxicity following CAR T cell infusion","authors":"Andrea Tavosanis","doi":"10.1038/s44161-025-00750-x","DOIUrl":"10.1038/s44161-025-00750-x","url":null,"abstract":"","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"4 11","pages":"1447-1447"},"PeriodicalIF":10.8,"publicationDate":"2025-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145472324","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-11-07DOI: 10.1038/s44161-025-00743-w
Mark W. Feinberg, Jorge Plutzky
Genome-wide association studies (GWAS) in coronary artery disease have revealed gene variants highly expressed in vascular smooth muscles cells (SMCs). Research now suggests that loss of one, Prdm16, drives a switch toward a synthetic SMC phenotype, with robust, potentially protective extracellular matrix production and fibrous cap formation.
{"title":"Flipping the PRDM16 switch in ‘multifunctional mesenchymes’ may help to define atherosclerotic plaque","authors":"Mark W. Feinberg, Jorge Plutzky","doi":"10.1038/s44161-025-00743-w","DOIUrl":"10.1038/s44161-025-00743-w","url":null,"abstract":"Genome-wide association studies (GWAS) in coronary artery disease have revealed gene variants highly expressed in vascular smooth muscles cells (SMCs). Research now suggests that loss of one, Prdm16, drives a switch toward a synthetic SMC phenotype, with robust, potentially protective extracellular matrix production and fibrous cap formation.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"4 11","pages":"1459-1461"},"PeriodicalIF":10.8,"publicationDate":"2025-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145472309","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-11-06DOI: 10.1038/s44161-025-00748-5
Gerburg Schwaerzer
{"title":"Cardiovascular-related complications in pregnancy have risen in the past decades","authors":"Gerburg Schwaerzer","doi":"10.1038/s44161-025-00748-5","DOIUrl":"10.1038/s44161-025-00748-5","url":null,"abstract":"","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"4 11","pages":"1450-1450"},"PeriodicalIF":10.8,"publicationDate":"2025-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145460882","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-11-04DOI: 10.1038/s44161-025-00741-y
Jacob G. Cox, Timothy A. McKinsey
Anthrax toxin receptor 1 (ANTXR1), an integrin-like transmembrane protein, is a docking platform for anthrax toxin and mediates cell–extracellular matrix interactions. New work shows that ANTXR1 stabilizes transforming growth factor-β receptors on cardiac fibroblasts, leading to profibrotic signaling and pathological remodeling of the heart.
{"title":"Waging war against cardiac fibrosis by targeting the anthrax toxin receptor","authors":"Jacob G. Cox, Timothy A. McKinsey","doi":"10.1038/s44161-025-00741-y","DOIUrl":"10.1038/s44161-025-00741-y","url":null,"abstract":"Anthrax toxin receptor 1 (ANTXR1), an integrin-like transmembrane protein, is a docking platform for anthrax toxin and mediates cell–extracellular matrix interactions. New work shows that ANTXR1 stabilizes transforming growth factor-β receptors on cardiac fibroblasts, leading to profibrotic signaling and pathological remodeling of the heart.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"4 11","pages":"1451-1453"},"PeriodicalIF":10.8,"publicationDate":"2025-11-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145446767","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-11-03DOI: 10.1038/s44161-025-00739-6
Andy Shing-Fung Chan, Joachim Greiner, Lisa Marschhäuser, Tomás A. Brennan, Stefanie Perez-Feliz, Ankit Agrawal, Helene Hemmer, Katrin Sinning, Jennifer Wing Lam Cheung, Zafar Iqbal, Alexander Klesen, Tamara Antonela Vico, Julieta Aprea, Ingo Hilgendorf, Thomas Seidel, Martin Vaeth, Eva A. Rog-Zielinska, Peter Kohl, Franziska Schneider-Warme, Dominic Grün
The heart is one of the least regenerative organs in humans, and ischemic heart disease is the leading cause of death worldwide. Understanding the cellular and molecular processes that occur during cardiac wound healing is an essential prerequisite to reducing health burden and improving cardiac function after myocardial tissue damage. Here, by integrating single-cell RNA sequencing with high-resolution spatial transcriptomics, we reconstruct the spatiotemporal dynamics of the fibrotic niches after cardiac injury in adult mice. We reveal a complex multicellular network that regulates cardiac repair, including fibroblast proliferation silencing by Trem2high macrophages to prevent excessive fibrosis. We further discovered a rare population of progenitor-like cardiomyocytes after lesion, promoted by myeloid and lymphoid niche signals. Culturing non-regenerative mouse cardiomyocytes or human heart tissue with these niche factors reactivated progenitor gene expression and cell cycle activity. In summary, this spatiotemporal atlas provides valuable insights into the heterocellular interactions that control cardiac repair. Chan et al. generate a high-resolution spatiotemporal atlas of healing hearts and reveal cellular networks of lesion repair, including macrophage–fibroblast interactions that control late-stage fibrosis and immune niches that induce cardiomyocyte de-differentiation.
{"title":"Spatiotemporal dynamics of the cardioimmune niche during lesion repair","authors":"Andy Shing-Fung Chan, Joachim Greiner, Lisa Marschhäuser, Tomás A. Brennan, Stefanie Perez-Feliz, Ankit Agrawal, Helene Hemmer, Katrin Sinning, Jennifer Wing Lam Cheung, Zafar Iqbal, Alexander Klesen, Tamara Antonela Vico, Julieta Aprea, Ingo Hilgendorf, Thomas Seidel, Martin Vaeth, Eva A. Rog-Zielinska, Peter Kohl, Franziska Schneider-Warme, Dominic Grün","doi":"10.1038/s44161-025-00739-6","DOIUrl":"10.1038/s44161-025-00739-6","url":null,"abstract":"The heart is one of the least regenerative organs in humans, and ischemic heart disease is the leading cause of death worldwide. Understanding the cellular and molecular processes that occur during cardiac wound healing is an essential prerequisite to reducing health burden and improving cardiac function after myocardial tissue damage. Here, by integrating single-cell RNA sequencing with high-resolution spatial transcriptomics, we reconstruct the spatiotemporal dynamics of the fibrotic niches after cardiac injury in adult mice. We reveal a complex multicellular network that regulates cardiac repair, including fibroblast proliferation silencing by Trem2high macrophages to prevent excessive fibrosis. We further discovered a rare population of progenitor-like cardiomyocytes after lesion, promoted by myeloid and lymphoid niche signals. Culturing non-regenerative mouse cardiomyocytes or human heart tissue with these niche factors reactivated progenitor gene expression and cell cycle activity. In summary, this spatiotemporal atlas provides valuable insights into the heterocellular interactions that control cardiac repair. Chan et al. generate a high-resolution spatiotemporal atlas of healing hearts and reveal cellular networks of lesion repair, including macrophage–fibroblast interactions that control late-stage fibrosis and immune niches that induce cardiomyocyte de-differentiation.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"4 11","pages":"1550-1572"},"PeriodicalIF":10.8,"publicationDate":"2025-11-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s44161-025-00739-6.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145440240","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-10-31DOI: 10.1038/s44161-025-00745-8
In cardiomyopathy caused by mutations in LMNA, which encodes the nuclear protein lamin A/C, cardiomyocyte nuclei are fragile and prone to rupture. This study reveals that this rupture arises from forces generated by a perinuclear microtubule cage, rather than from sarcomere contraction. Targeting microtubule–nuclei interactions might offer a therapeutic strategy to preserve cardiac function.
{"title":"A microtubule cage damages weakened nuclei in a genetic cardiomyopathy","authors":"","doi":"10.1038/s44161-025-00745-8","DOIUrl":"10.1038/s44161-025-00745-8","url":null,"abstract":"In cardiomyopathy caused by mutations in LMNA, which encodes the nuclear protein lamin A/C, cardiomyocyte nuclei are fragile and prone to rupture. This study reveals that this rupture arises from forces generated by a perinuclear microtubule cage, rather than from sarcomere contraction. Targeting microtubule–nuclei interactions might offer a therapeutic strategy to preserve cardiac function.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"4 11","pages":"1464-1465"},"PeriodicalIF":10.8,"publicationDate":"2025-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145423725","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-10-27DOI: 10.1038/s44161-025-00734-x
Emily S. Lau
Physical activity lowers the risk of cardiovascular disease and overall mortality. Research now shows that women may derive greater cardiovascular benefit from exercise than men.
{"title":"Sex differences in the association of physical activity with coronary heart disease incidence and mortality","authors":"Emily S. Lau","doi":"10.1038/s44161-025-00734-x","DOIUrl":"10.1038/s44161-025-00734-x","url":null,"abstract":"Physical activity lowers the risk of cardiovascular disease and overall mortality. Research now shows that women may derive greater cardiovascular benefit from exercise than men.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"4 11","pages":"1457-1458"},"PeriodicalIF":10.8,"publicationDate":"2025-10-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145380026","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-10-27DOI: 10.1038/s44161-025-00732-z
Jiajin Chen, Yuliang Wang, Zihang Zhong, Xin Chen, Le Zhang, Lingjun Jie, Yangyang Zhang, Yan Wang
Despite American Heart Association, European Society of Cardiology and World Health Organization (AHA/ESC/WHO) guidelines uniformly recommending 150 min week−1 of moderate-to-vigorous physical activity (MVPA) for both sexes, a substantial ‘gender gap’ persists in exercise capacity and guideline adherence, and its impact on coronary heart disease (CHD) development and prognosis remains underexplored. Here we analyzed the accelerometer-measured MVPA of 80,243 CHD-free participants to assess CHD incidence and 5,169 patients with CHD to evaluate all-cause mortality. Compared with non-adherent counterparts, guideline-adherent participants showed a 22% lower CHD risk in female individuals (hereinafter referred to as females) and a 17% lower CHD risk in male individuals (hereinafter referred to as males; (Pinteraction = 0.009). Notably, females achieved a CHD risk reduction of 30% (hazard ratio (HR) = 0.70) with 250 min week−1 of MVPA, whereas males required 530 min week−1 for comparable benefits. Among patients with CHD, active females experienced greater mortality risk reduction than males (HR = 0.30 versus 0.81; Pinteraction = 0.004). Similar sex differences were observed when analyzing guideline-adhering days (Pinteraction < 0.05). Our findings underscore the value of sex-specific tailored CHD prevention strategies using wearable devices, which may help bridge the ‘gender gap’ by motivating females to engage in physical activity. Chen, Wang, Zhong and colleagues show that females derive greater cardiovascular benefits from guideline-recommended levels of physical activity and require less activity than males to see their beneficial effects.
{"title":"Sex differences in the association of wearable accelerometer-derived physical activity with coronary heart disease incidence and mortality","authors":"Jiajin Chen, Yuliang Wang, Zihang Zhong, Xin Chen, Le Zhang, Lingjun Jie, Yangyang Zhang, Yan Wang","doi":"10.1038/s44161-025-00732-z","DOIUrl":"10.1038/s44161-025-00732-z","url":null,"abstract":"Despite American Heart Association, European Society of Cardiology and World Health Organization (AHA/ESC/WHO) guidelines uniformly recommending 150 min week−1 of moderate-to-vigorous physical activity (MVPA) for both sexes, a substantial ‘gender gap’ persists in exercise capacity and guideline adherence, and its impact on coronary heart disease (CHD) development and prognosis remains underexplored. Here we analyzed the accelerometer-measured MVPA of 80,243 CHD-free participants to assess CHD incidence and 5,169 patients with CHD to evaluate all-cause mortality. Compared with non-adherent counterparts, guideline-adherent participants showed a 22% lower CHD risk in female individuals (hereinafter referred to as females) and a 17% lower CHD risk in male individuals (hereinafter referred to as males; (Pinteraction = 0.009). Notably, females achieved a CHD risk reduction of 30% (hazard ratio (HR) = 0.70) with 250 min week−1 of MVPA, whereas males required 530 min week−1 for comparable benefits. Among patients with CHD, active females experienced greater mortality risk reduction than males (HR = 0.30 versus 0.81; Pinteraction = 0.004). Similar sex differences were observed when analyzing guideline-adhering days (Pinteraction < 0.05). Our findings underscore the value of sex-specific tailored CHD prevention strategies using wearable devices, which may help bridge the ‘gender gap’ by motivating females to engage in physical activity. Chen, Wang, Zhong and colleagues show that females derive greater cardiovascular benefits from guideline-recommended levels of physical activity and require less activity than males to see their beneficial effects.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"4 11","pages":"1539-1549"},"PeriodicalIF":10.8,"publicationDate":"2025-10-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s44161-025-00732-z.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145380078","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-10-17DOI: 10.1038/s44161-025-00737-8
Josephine M. E. Tan, Lan Cheng, Ryan P. Calhoun, Angela H. Weller, Karima Drareni, Skylar Fong, Eirlys Barbara, Hee-Woong Lim, Chenyi Xue, Hanna Winter, Gaëlle Auguste, Clint L. Miller, Muredach P. Reilly, Lars Maegdefessel, Esther Lutgens, Patrick Seale
Vascular smooth muscle cells (SMCs) undergo phenotype switching to acquire various fates in response to pathological stimuli. Among these, ‘synthetic’ SMCs—defined by migration, proliferation and extracellular matrix production—accumulate in atherosclerotic lesions and contribute to fibrous cap formation. The mechanisms driving this synthetic transition remain unclear. Here we identify PRDM16, a gene linked to cardiovascular disease, as a critical transcriptional repressor of the synthetic SMC phenotype. PRDM16 expression declined during SMC modulation, and its deletion in mice induced a synthetic program across all SMC subtypes even without pathological stimuli. Under atherogenic conditions, PRDM16 deficiency resulted in the formation of fibroproliferative plaques with more synthetic SMCs and fewer foam cells. Conversely, enforced PRDM16 expression suppressed SMC migration, proliferation and fibrosis. Mechanistically, PRDM16 occupied chromatin and suppressed activating marks at synthetic loci. These findings establish PRDM16 as a gatekeeper of SMC fate and reveal its role in shaping atherosclerotic plaque composition. Tan et al. identify PRDM16 as a key repressor of fibrotic switching in smooth muscle cells and show that its downregulation in atherosclerosis drives smooth muscle cells toward a synthetic fate, promoting fibrous plaques.
{"title":"PRDM16 regulates smooth muscle cell identity and atherosclerotic plaque composition","authors":"Josephine M. E. Tan, Lan Cheng, Ryan P. Calhoun, Angela H. Weller, Karima Drareni, Skylar Fong, Eirlys Barbara, Hee-Woong Lim, Chenyi Xue, Hanna Winter, Gaëlle Auguste, Clint L. Miller, Muredach P. Reilly, Lars Maegdefessel, Esther Lutgens, Patrick Seale","doi":"10.1038/s44161-025-00737-8","DOIUrl":"10.1038/s44161-025-00737-8","url":null,"abstract":"Vascular smooth muscle cells (SMCs) undergo phenotype switching to acquire various fates in response to pathological stimuli. Among these, ‘synthetic’ SMCs—defined by migration, proliferation and extracellular matrix production—accumulate in atherosclerotic lesions and contribute to fibrous cap formation. The mechanisms driving this synthetic transition remain unclear. Here we identify PRDM16, a gene linked to cardiovascular disease, as a critical transcriptional repressor of the synthetic SMC phenotype. PRDM16 expression declined during SMC modulation, and its deletion in mice induced a synthetic program across all SMC subtypes even without pathological stimuli. Under atherogenic conditions, PRDM16 deficiency resulted in the formation of fibroproliferative plaques with more synthetic SMCs and fewer foam cells. Conversely, enforced PRDM16 expression suppressed SMC migration, proliferation and fibrosis. Mechanistically, PRDM16 occupied chromatin and suppressed activating marks at synthetic loci. These findings establish PRDM16 as a gatekeeper of SMC fate and reveal its role in shaping atherosclerotic plaque composition. Tan et al. identify PRDM16 as a key repressor of fibrotic switching in smooth muscle cells and show that its downregulation in atherosclerosis drives smooth muscle cells toward a synthetic fate, promoting fibrous plaques.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"4 11","pages":"1573-1588"},"PeriodicalIF":10.8,"publicationDate":"2025-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s44161-025-00737-8.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145314214","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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