Nature Reviews Cardiology最新文献_第10页

Neuroimmune circuits drive pathological remodelling after myocardial infarction 心肌梗死后神经免疫回路驱动病理重构。

IF 44.2 1区医学

Nature Reviews Cardiology Pub Date : 2026-01-29 DOI: 10.1038/s41569-026-01258-y

Gregory B. Lim

引用次数: 0

The environmental exposome in heart failure risk and progression 环境暴露对心力衰竭风险和进展的影响。

IF 50.2 1区医学

Nature Reviews Cardiology Pub Date : 2026-01-26 DOI: 10.1038/s41569-026-01247-1

Omar Hahad, Sojin Wass, Sanjay Rajagopalan, Shady Abohashem, Hua Hao, Ana Navas-Acien, Lavanya Bellumkonda, Kai Chen, Robert D. Brook, Khurram Nasir, Philipp Lurz, David E. Lanfear, Arvind Bhimaraj, Sadeer Al-Kindi

{"title":"The environmental exposome in heart failure risk and progression","authors":"Omar Hahad, Sojin Wass, Sanjay Rajagopalan, Shady Abohashem, Hua Hao, Ana Navas-Acien, Lavanya Bellumkonda, Kai Chen, Robert D. Brook, Khurram Nasir, Philipp Lurz, David E. Lanfear, Arvind Bhimaraj, Sadeer Al-Kindi","doi":"10.1038/s41569-026-01247-1","DOIUrl":"10.1038/s41569-026-01247-1","url":null,"abstract":"Environmental exposures have a crucial role in the incidence and progression of heart failure (HF) by exacerbating genetic predisposition and other pathophysiological mechanisms. The exposome — encompassing pollution, climate and the urban environment — and the biological responses to these factors shape cardiovascular health in complex ways. Air, noise and light pollution, exposure to toxic metals, and extremes of temperature adversely affect HF outcomes. Social determinants of health, including socioeconomic status, amplify these environmental risks, disproportionately affecting vulnerable populations. Conversely, green spaces and walkable neighbourhoods are linked to a reduced risk of HF, improved vascular health and medication adherence. Emerging evidence suggests that environmental stressors influence HF outcomes from early life by altering gene expression through epigenetic mechanisms. Despite these insights, research gaps remain. Future studies must integrate environmental, genetic and multiomics data to refine risk prediction and guide targeted public health interventions. A comprehensive understanding of the exposome in the aetiology of HF is essential for developing prevention strategies that address both biological and social determinants of cardiovascular health. The environmental exposome, which includes pollution, contamination, climate and social determinants of health, is intricately involved in the pathophysiology of heart failure. In this Review, Hahad and colleagues explore the complex relationship between environmental stressors and heart failure, advocating for their inclusion alongside traditional risk factors and highlighting the need for new strategies to address the effects of the exposome on public health.","PeriodicalId":18976,"journal":{"name":"Nature Reviews Cardiology","volume":"23 7","pages":"457-472"},"PeriodicalIF":50.2,"publicationDate":"2026-01-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146044599","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}

引用次数: 0

Residual cardiovascular risk in coronary artery disease: from pathophysiology to established and novel therapies 冠状动脉疾病的剩余心血管风险：从病理生理学到现有的和新的治疗方法

IF 50.2 1区医学

Nature Reviews Cardiology Pub Date : 2026-01-23 DOI: 10.1038/s41569-026-01249-z

Mattia Galli, Antonio Abbate, Marc P. Bonaca, Filippo Crea, Maurizio Forte, Giacomo Frati, Mario Gaudino, C. Michael Gibson, Diana A. Gorog, Roxana Mehran, Rocco A. Montone, Michelle L. O’Donoghue, P. Gabriel Steg, Sebastiano Sciarretta, Dominick J. Angiolillo

{"title":"Residual cardiovascular risk in coronary artery disease: from pathophysiology to established and novel therapies","authors":"Mattia Galli, Antonio Abbate, Marc P. Bonaca, Filippo Crea, Maurizio Forte, Giacomo Frati, Mario Gaudino, C. Michael Gibson, Diana A. Gorog, Roxana Mehran, Rocco A. Montone, Michelle L. O’Donoghue, P. Gabriel Steg, Sebastiano Sciarretta, Dominick J. Angiolillo","doi":"10.1038/s41569-026-01249-z","DOIUrl":"10.1038/s41569-026-01249-z","url":null,"abstract":"Despite substantial advances in the secondary prevention of cardiovascular disease, atherosclerosis of the coronary arteries and its consequences remain the leading cause of death worldwide. Residual cardiovascular risk refers to the ongoing risk of recurrent cardiovascular events that persists in patients with coronary artery disease despite receiving optimal secondary prevention treatment and effective control of conventional risk factors. Lifestyle modification and therapies modulating thrombosis, blood pressure and LDL-cholesterol levels represent the standard approach for the prevention of recurrent cardiovascular events in patients with coronary artery disease. However, current evidence-based therapies and lifestyle modification strategies only partially modulate the pathophysiological pathways involved in the progression and destabilization of atherosclerotic disease, and other mechanisms might have an important role, accounting, at least in part, for the residual cardiovascular risk in these patients. In this Review, we appraise the available evidence and latest insights into the mechanisms and associated biomarkers of recurrent adverse cardiovascular events and provide perspectives on strategies to reduce residual cardiovascular risk in patients with coronary artery disease. In this Review, Galli and colleagues discuss the mechanisms and associated biomarkers of traditional and emerging factors responsible for the residual risk of recurrent adverse cardiovascular events in patients with coronary artery disease, with a focus on new pathophysiological insights and the therapeutic implications.","PeriodicalId":18976,"journal":{"name":"Nature Reviews Cardiology","volume":"23 7","pages":"500-523"},"PeriodicalIF":50.2,"publicationDate":"2026-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146032821","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}

引用次数: 0

Low-dose IL-2 therapy reduces arterial inflammation in acute coronary syndromes 低剂量IL-2治疗可减少急性冠状动脉综合征的动脉炎症。

IF 44.2 1区医学

Nature Reviews Cardiology Pub Date : 2026-01-22 DOI: 10.1038/s41569-026-01256-0

Irene Fernández-Ruiz

引用次数: 0

Molecular damage associated with ageing drives inflammation in cardiovascular disease 与衰老相关的分子损伤导致心血管疾病的炎症。

IF 50.2 1区医学

Nature Reviews Cardiology Pub Date : 2026-01-22 DOI: 10.1038/s41569-026-01253-3

Allison B. Herman, Julián Candia, David M. Wilson III, Stefano Donega, Martin Picard, Luigi Ferrucci

{"title":"Molecular damage associated with ageing drives inflammation in cardiovascular disease","authors":"Allison B. Herman, Julián Candia, David M. Wilson III, Stefano Donega, Martin Picard, Luigi Ferrucci","doi":"10.1038/s41569-026-01253-3","DOIUrl":"10.1038/s41569-026-01253-3","url":null,"abstract":"Chronic inflammation has long been recognized as a major risk factor for and a causal contributor to cardiovascular disease (CVD). However, advances in omics technologies and deepening insights into CVD pathogenesis have expanded our understanding of the underlying mechanisms. Inflammation is now seen not as an isolated cause, but as one of several biological responses to cumulative tissue damage over time. In this Review, we propose that inflammation initially functions as a resilience mechanism, acting to resolve molecular and cellular damage driven by environmental stressors and intrinsic age-related entropy. With ageing, however, this protective response can become dysregulated and maladaptive, promoting collateral pathological changes. We illustrate this theory through two examples, atherosclerosis and age-related impairment of tissue perfusion, and support these conceptual models using proteomic data from large population studies with cardiovascular outcomes. Our findings reaffirm the central role of inflammation in CVD pathophysiology, but also indicate that the upstream biological driver of inflammation is molecular damage that is either not readily prevented or repaired by inadequate resilience mechanisms. Understanding the coordination of these responses offers new opportunities for targeted prevention and treatment of CVD. In this Review, Ferrucci and colleagues propose that inflammation is a resilience mechanism that resolves molecular and cellular damage driven by environmental stressors. With ageing, however, this protective response can become dysregulated and maladaptive, promoting collateral changes central to the pathophysiology of cardiovascular disease.","PeriodicalId":18976,"journal":{"name":"Nature Reviews Cardiology","volume":"23 7","pages":"486-499"},"PeriodicalIF":50.2,"publicationDate":"2026-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146021675","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}

引用次数: 0

Reply to: ‘The use of β-blockers after myocardial infarction: no doubts remain’ 回复：“心肌梗死后β受体阻滞剂的使用：毫无疑问”。

IF 44.2 1区医学

Nature Reviews Cardiology Pub Date : 2026-01-19 DOI: 10.1038/s41569-026-01251-5

John G. F. Cleland

引用次数: 0

The use of β-blockers after myocardial infarction: no doubts remain 心肌梗死后β受体阻滞剂的使用：毫无疑问。

IF 44.2 1区医学

Nature Reviews Cardiology Pub Date : 2026-01-19 DOI: 10.1038/s41569-026-01252-4

Dan Atar, John Munkhaugen, Eva Irene Bossano Prescott, Tomas Jernberg, Borja Ibáñez

引用次数: 0

Procoagulant platelets: linking coagulation and thromboinflammation in cardiovascular disease 促凝血小板：心血管疾病中凝血和血栓炎症的联系。

IF 50.2 1区医学

Nature Reviews Cardiology Pub Date : 2026-01-14 DOI: 10.1038/s41569-026-01250-6

Rainer Kaiser, Leo Nicolai

{"title":"Procoagulant platelets: linking coagulation and thromboinflammation in cardiovascular disease","authors":"Rainer Kaiser, Leo Nicolai","doi":"10.1038/s41569-026-01250-6","DOIUrl":"10.1038/s41569-026-01250-6","url":null,"abstract":"Platelets are the key cell types in haemostasis after vascular injury and crucially contribute to thrombus formation. In addition to their aggregation and clot contraction functions after stimulation by soluble agonists or extracellular matrix proteins, platelets can adopt a highly activated state known as procoagulant activation. Procoagulant platelets influence the pathophysiology underlying various cardiovascular diseases, including myocardial infarction, stroke and deep vein thrombosis. Findings described in the past decade position procoagulant platelets at the dynamic intersection between thrombosis and inflammation. In this Review, we discuss the expanding research on procoagulant platelets, describing how this platelet activation state contributes to macrovascular and microvascular clot formation in cardiovascular diseases. We summarize the key receptors and signalling pathways that control platelet procoagulant activation and that distinguish the procoagulant phenotype from other platelet activation states. Finally, we highlight the clinical significance of platelet procoagulant activation and discuss how the individual pathways involved in this activation can be targeted with the use of both readily available and novel therapeutic approaches, providing a framework for future research that might lead to new diagnostic and therapeutic applications in cardiovascular disease, septic inflammation and immune complex-mediated diseases. In this Review, Kaiser and Nicolai summarize our understanding of procoagulant platelets, describing the signalling pathways that control platelet procoagulant activation and discussing the role of procoagulant platelets in venous and arterial thrombosis, as well as potential therapeutic approaches to target these platelets in thrombotic and thromboinflammatory disorders, including cardiovascular disease, septic inflammation and immune complex-mediated diseases.","PeriodicalId":18976,"journal":{"name":"Nature Reviews Cardiology","volume":"23 7","pages":"473-485"},"PeriodicalIF":50.2,"publicationDate":"2026-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145968384","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}

引用次数: 0

Oral anticoagulant therapy after ablation for atrial fibrillation 房颤消融后口服抗凝治疗。

IF 44.2 1区医学

Nature Reviews Cardiology Pub Date : 2026-01-12 DOI: 10.1038/s41569-026-01248-0

Giulio Francesco Romiti, Marco Proietti

引用次数: 0

Robotic cardiac surgery: past, present and future 机器人心脏手术：过去，现在和未来。

IF 44.2 1区医学

Nature Reviews Cardiology Pub Date : 2026-01-02 DOI: 10.1038/s41569-025-01246-8

David W. Miranda, Omar Toubat, Michael Ibrahim

引用次数: 0