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Nature Cardiovascular Research

Publisher:
Springer Nature
ISSN:
2731-0590
Category:
CARDIAC & CARDIOVASCULAR SYSTEMS
Impact factor:
9.4

Feed status

15 parsed articles

Last update: Not fetched

Latest articles

Immature neutrophils sound the alarm in acute myocardial infarction

2026-07-23

Alexander J. F. Thurston

Nature Cardiovascular Research, Published online: 23 July 2026; doi:10.1038/s44161-026-00848-w Myocardial infarction can cause lasting cardiac damage, heart failure and death, and immune responses are increasingly recognized as key determinants of outcomes. A study now shows that ST-segment elevation myocardial infarction (STEMI) mobilizes immature neutrophil progenitors from the bone marrow, predicting increased mortality risk.]]>

DOI: 10.1038/s44161-026-00848-w

Mavacamten shows broad benefit in human and mouse models of MYBPC3 -related hypertrophic cardiomyopathy

2026-07-07

Laura Sen-Martín

Nature Cardiovascular Research, Published online: 07 July 2026; doi:10.1038/s44161-026-00833-3 Sen-Martín et al. demonstrate that mavacamten exerts therapeutic benefit in hypertrophic cardiomyopathy caused by both missense and truncating MYBPC3 variants by reducing hypercontractility and myocardial remodeling through normalization of myosin activity.]]>

DOI: 10.1038/s44161-026-00833-3

Proteomics reveals spatial and molecular heterogeneities in advanced atherosclerotic carotid artery plaques

2026-06-22

Ankit Sinha

Nature Cardiovascular Research, Published online: 22 June 2026; doi:10.1038/s44161-026-00827-1 Atherosclerotic plaque rupture underlies many cerebrovascular events, yet the molecular determinants of vulnerable plaque morphology remain poorly defined. Using histomorphology-guided spatial proteomics of 112 carotid plaques, Sinha et al. show that cap thickness-associated molecular programs are spatially confined to the fibrous cap and necrotic core, link thin-cap plaques to inflammatory and lipid handling pathways, and identify PCSK9 as a compartment-specific marker induced by oxidative and inflammatory stress in vascular smooth muscle cells.]]>

DOI: 10.1038/s44161-026-00827-1

CAMK2 inhibition treats genetic dilated cardiomyopathy in mice

2026-05-21

Nature Cardiovascular Research, Published online: 21 May 2026; doi:10.1038/s44161-026-00826-2 Pathogenic variants in RBM20, which encodes a cardiac splicing factor, lead to an aggressive form of dilated cardiomyopathy with a high risk of ventricular arrhythmias. This study shows that genetic or pharmacological inhibition of CAMK2D, one of the RBM20 splicing targets, rescues cardiac dysfunction in mouse models of RBM20.]]>

DOI: 10.1038/s44161-026-00826-2

Multi-view deep learning for echocardiogram interpretation

2026-03-17

Mostafa A. Al-Alusi

Nature Cardiovascular Research, Published online: 17 March 2026; doi:10.1038/s44161-026-00780-z Deep learning can identify cardiac abnormalities from echocardiogram videos, but previous work has predominantly used 2D video clips from a single cross-section of the heart. Research now shows that more complex approaches that integrate information from several echocardiographic views can improve deep learning prediction of cardiac abnormalities.

Decentralized clinical trials in cardiovascular disease : A primer for clinical trialists

2026-03-17

Guillaume Baudry, Prashanth Kulkarni, Tor Biering-Sørensen, Adam D. DeVore, Charles Michael Gibson, Christopher B. Granger, Harriette G. C. Van Spall

Nature Cardiovascular Research, Published online: 17 March 2026; doi:10.1038/s44161-026-00788-5 Baudry et al. review the main components and operational considerations for running decentralized clinical trials, outline their specific advantages for the cardiovascular field, and propose strategies to mitigate their downsides and ensure their quality.

Hematopoietic expression of cIAP2 drives inflammation and heart failure after myocardial infarction

2026-03-12

David Smyth, Liyong Zhang, Mohammad Al-Khalaf, Sabrina Robichaud, Richard Seymour, Michele Geoffrion, Richard Jung, Simon Parlow, Feng Du, Brian McNeill, Qiujiang Du, Caroline Beauregard, Xiaoling Zhao, Mireille Ouimet, Shawn T. Beug, Eric C. LaCasse, Katey J. Rayner, Tak W. Mak, Benjamin Hibbert, Robert G. Korneluk, Peter P. Liu

Nature Cardiovascular Research, Published online: 12 March 2026; doi:10.1038/s44161-026-00782-x Smyth et al. demonstrate that a cellular inhibitor of apoptosis, cIAP2, exacerbates inflammation and cardiac injury after myocardial infarction and that its inhibition, either genetically or via Smac mimetics, offers a promising immunotherapeutic strategy to reduce post-MI damage and progression to heart failure.