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In mouse models of atherosclerosis, smooth muscle cell (SMC)-specific disruption of a gene associated with coronary artery disease in human genome-wide association studies alters atherosclerotic plaque features by promoting SMC transition to an atherogenic phenotype.
Genome-wide association studies of magnetic resonance imaging (MRI) of diastolic heart function shed light on the underlying molecular mechanisms and support a causal role of diastolic function for the development of heart failure.
In this Review, Banning and colleagues summarize diagnostic techniques that assess microcirculation in each specific organ, critically appraise all the evidence that supports the systemic and multi-organ nature of microvascular dysfunction and focus on current and emerging interventions for the treatment of microvascular dysfunction.
In this Review, Bowers et al. discuss how the development of therapeutics to combat cardiac diseases, specifically fibrosis, relies on a deeper understanding of how the cardiac extracellular matrix is intertwined with signaling processes that underlie cardiac cell activation and behavior.
A combined imaging–clinical risk prediction model with the use of deep learning seems a promising approach for predicting sudden cardiac death in patients with ischemic cardiomyopathies. Deep-learning-guided clinical trials will be needed to translate this model into clinical practice.
Global or macrophage-specific knockout of Trpm2, which encodes the calcium-permeable ion channel TRPM2, protects mice against atherosclerosis induced by a high-fat diet. Mechanistically, activation of TRPM2 and the scavenger receptor CD36 promote the transformation of macrophages into inflammatory foam cells, thereby accelerating the development and progression of atherosclerosis.
ABCA1 promotes the efflux of cholesterol from cells to HDL and has anti-atherogenic activities. Sun and Li present cryo-EM structures of ABCA1 in the ATP-free and ATP-bound states, which reveal bound cholesterol molecules and suggest a transmembrane cholesterol-transport mechanism.
Mauro Giacca and Ajay M. Shah discuss the most recent advances in the bidirectional relationship between COVID-19 and an array of cardiovascular diseases.
Joseph A. Hill and colleagues discuss basic and translational data focusing on the most common form of heart failure with preserved ejection fraction (HFpEF), cardiometabolic HFpEF, emphasizing the bidirectional cross-talk between metabolic dysregulation triggering immune events—and vice versa—in syndrome pathogenesis.
Statins continue to make a difference and are here to stay. A new study provides further evidence that statins can function beyond inhibition of cholesterol synthesis by increasing the rate of macrophage efferocytosis, via a reduction in the ‘don’t eat me’ signal CD47, thereby decreasing the atherosclerotic plaque burden.
In this Review, Hwa and colleagues summarize the latest advances in platelet biology and function and appraise the technical and biological challenges in platelet investigations.
The International Mouse Phenotyping Consortium releases cardiac phenotype characterization of almost 4,000 monogenic null mice. This impressive international effort reports 486 new genes associated with cardiac malfunction.
High frequency of depressed mood increases the risk of future cardiometabolic disease above that due to lifestyle factors and genetic susceptibility alone, raising new questions about risk management in individuals susceptible to depression.
Alan Tall and Jose Fuster review the latest advances in our knowledge of the function of clonal hematopoiesis in cardiovascular disease and discuss the translation of this knowledge into therapeutics.
Barisano et al. discuss how vascular dysfunction caused by blood–brain barrier breakdown interacts with amyloid beta and tau AD biomarkers and may predict early cognitive impairment, dementia and Alzheimer’s disease.
Aortic-intima-resident macrophages (MACAIRs) share the vessel luminal lining with endothelial cells in areas of turbulent flow and protrude into the arterial blood stream to clean the inner arterial surface via phagocytosis, shield nearby endothelial cells from activation by thrombin and prevent microthrombus formation.
In this issue of Nature Cardiovascular Research, Aung and colleagues1 use breathalyser data to identify dates associated with high concentrations of blood alcohol, which matched days with excess emergency department presentations for atrial fibrillation. This study strengthens the existing evidence that binge drinking is responsible for atrial fibrillation in ‘holiday heart’.
This Review discusses the physical concepts and descriptions of the structures that determine myocardial stiffness, different techniques used to estimate myocardial stiffness, and their application in clinical medicine.
