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Acute ischaemic stroke induces persistent innate immune memory through epigenetic changes in myeloid progenitors in the bone marrow, and this innate immune training contributes to cardiac remodelling and dysfunction in the long term, according to a new study.
A new study indicates that proteins in the sarcomere complex are stochastically removed and degraded and are replaced by newly translated proteins. Sarcomere turnover occurs at a similar rate within cardiomyocytes and across the heart and slows with ageing.
Preliminary experience with the use of transcatheter aortic valve implantation (TAVI) to treat non-calcific aortic regurgitation has raised concerns about the short-term effectiveness of TAVI in this setting. A deeper understanding of the interaction between transcatheter heart valves and anatomy in patients with non-calcific aortic valve disease, coupled with the introduction of dedicated TAVI devices, is providing new opportunities in the management of this condition.
The advent of pulsed-field ablation — a series of ultra-rapid, high-energy pulses that result in non-thermal cell death via electroporation — is revolutionizing the field of atrial fibrillation ablation. Data on first iterations of the technology indicate that safety and efficacy are at least similar to that of thermal ablation but with meaningfully shorter procedure duration.
In this Tools of the Trade article, Berkeley and Thomson describe the use of a minimally invasive strategy to standardize the induction of myocardial infarction in mice.
In this Tools of the Trade article, Jablonska describes the use of proximity-based labelling for the proteomic profiling of novel protein–protein interactions.
Findings from a new study published in Science Immunology suggest that epigenetic changes in haematopoietic stem cells promote the production of pro-inflammatory macrophages and influence their capacity to generate protective macrophage subsets.
Data from the phase IIb MUIR and ARCHES-2 trials show that RNA interference approaches that target either apolipoprotein C-III or ANGPTL3 significantly reduce plasma triglyceride levels in patients with mixed hyperlipidaemia.
Haemophilia A is caused by variants in the gene that encodes coagulation factor VIII (FVIII). Sequencing of this gene in the 1980s was the initial step in developing replacement therapy with recombinant FVIII, and thereby removing the risk of blood-borne infections from plasma-derived FVIII.
Corey McAleese describes the study that identified the presence of metabolic heterogeneity in endothelial cells from different tissues and discusses its relevance to our current understanding of endothelial metabolism.
Milda Folkmanaite and Manuela Zaccolo highlight a study that demonstrates a role for phase-separated condensates of protein kinase A in buffering molecules of cAMP, to illustrate how phase separation of proteins in cardiac cells might contribute to the regulation of cardiac function.
Poscablo and colleagues identify a distinct haematopoietic platelet differentiation pathway that is enriched in ageing mice, which results in platelets that are hyper-reactive compared with canonical platelet populations.
In patients with type 2 diabetes mellitus and obesity, bariatric metabolic surgery is associated with a lower risk of the incidence of first-ever congestive heart failure than treatment with glucagon-like peptide 1 receptor agonists, according to a new study.
Data from the SEQUOIA-HCM trial show that aficamten, a cardiac myosin inhibitor, increases exercise capacity and improves quality of life in patients with symptomatic obstructive hypertrophic cardiomyopathy.
A study in Nature describes a single-cell-type strategy for vascular cell therapies that involves the artificial transplantation of mitochondria to endothelial cells, which promotes mitophagy and facilitates the formation of functional vessels in ischaemic tissue without the need for mesenchymal stromal cell support.
Activation of the bile acid receptor TGR5 inhibits CD36-mediated fatty acid uptake in cardiomyocytes and protects against cardiac lipotoxicity and the development of diabetic cardiomyopathy in mice, according to a new study.
In the AEGIS-II trial, infusion of apolipoprotein A-I to increase cholesterol efflux capacity did not improve outcomes in patients with acute myocardial infarction.
