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By single-cell mass cytometry and adoptive transfer of B cell subtypes in mice, Pattarabanjird et al. show that human CD24hi circulating marginal zone B cells produce IgM to atherosclerosis antigens and confer atheroprotection. Blocking CD24 increased vascular inflammation in hyperlipidemic humanized mice.
Patterson, Firulyova, et al. report that TREM2 is a key regulator of foamy macrophage differentiation. Myeloid-specific deletion of Trem2 caused increased macrophage susceptibility to cholesterol-mediated toxicity and cell death and significantly attenuated atherosclerotic plaque progression in mice.
Abd Alla et al. identify bublin coiled-coil protein (BBLN) as a factor upregulated in unrepaired hearts of patients with tetralogy of Fallot, and show that this protein binds to and controls the function of calcium/calmodulin-dependent protein kinase II delta (CAMK2D). Overexpression of BBLN in mice induced pathological cardiac remodeling, which was precluded when the interaction of BBLN with CAMK2D was prevented or upon CAMK2D downregulation.
The results of EMPATROPISM-FE, a post hoc analysis of the EMPA-TROPISM trial performed by Angermann et al., suggest that the beneficial effects of empagliflozin treatment in heart failure populations may be related to changes in iron metabolism.
Loescher, Freundt et al. investigated the contribution of each cytoskeletal filament to passive myocardial stiffness by using a mouse model that allows for specific cleavage of titin; they show that titin is a major cytoskeletal filament controlling myocardial elastic forces, whereas viscous forces are controlled by titin, the microtubules and actin.
Xie et al. characterize the translational dynamics of fibroblast conversion into induced cardiomyocytes (iCMs) and identify the protein Ybx1 as a critical barrier to iCM transdifferentiation. Ybx1 protein removal in mice with myocardial infarction enhanced iCM conversion and rescued cardiac dysfunction.
Sweat, Cao et al. used different genetic and epigenetic approaches to show that Tbx5 is essential for the maintenance of atrial identity in postnatal cardiomyocytes by binding atrial-specific enhancers and maintaining the atrial-specific chromatin architecture, in a dose-dependent manner.
Lipov et al. performed a meta-analysis of biallelic genotypes in cardiomyopathy patients and the UK Biobank. Using rare variant association analysis, they identified 18 genes with robust evidence for recessive inheritance and revealed a complex spectrum of dominance and recessiveness.
Kwartler et al. show that α-smooth muscle actin functions in the nucleus by associating with chromatin remodeling complexes and the promoters of smooth muscle-specific genes, but this nuclear activity is reduced in ACTA2 p.Arg179 pathogenic variants, resulting in impaired smooth muscle differentiation and increased plasticity.
Khassafi et al. identify molecular subgroups of right ventricular (RV) dysfunction using transcriptomic analysis of RV samples from individuals with compensated RV hypertrophy or decompensated RV failure and two rat models of RV dysfunction. Several extracellular matrix genes found to be deregulated in decompensated RV subgroups were validated at the protein level in two independent cohorts of individuals with pulmonary arterial hypertension, revealing their predictive biomarker potential in maladaptive RV development.
Eberhardt et al. show that SARS-CoV-2 infects human coronary lesions where it preferentially targets plaque macrophages, triggering plaque inflammation and potentially leading to acute cardiovascular complications and long-term cardiovascular risks in patients with COVID-19.
C-C chemokine receptor type 2 (CCR2) is expressed on inflammatory populations of monocytes and macrophages that contribute to heart failure. In this study, Lavine et al. establish the feasibility of CCR2 imaging in patients who have had a myocardial infarction.
Abplanalp et al. define the transcriptome of cells carrying mutations in a specific gene at a single-cell level (MutDetect-Seq) and apply it to reveal the cell-intrinsic effects of mutations in DNMT3A associated with clonal hematopoiesis in patients with heart failure.
Rauch et al. show that loss-of-function mutations in the epigenetic regulator Dnmt3a lead to accelerated atherosclerosis, as previously shown for Tet2, and that loss of either gene leads to similar changes in atheroma composition, with the emergence of a distinct population of chemokine-enriched, resident-like macrophages infiltrating the adventitia, as revealed by single-cell transcriptomics and spatial proteomic analyses.
de Jonckheere, Kollotzek, et al. report a quantitative proteomic and lipidomic map of different stages of megakaryopoiesis and find an anionic lipid membrane remodeling and concomitant relocalization of the CKIP-1/CK2α complex to the plasma membrane of maturing megakaryocytes, which appear to be essential for sufficient platelet biogenesis.
Lin et al. show that MCM8 protects vascular health by mediating nitric-oxide-dependent mitophagy. The common East-Asian MCM8-P276 variant is ineffective in mitophagy, which potentiates cGAS-STING and type I interferon signaling in a mouse model of Kawasaki disease.
Han, Fang et al. show that the deubiquitinase JOSD2 deubiquitinates and stabilizes SERCA2a in cardiomyocytes, which results in normalized calcium handling and reduced cardiac pathology under hypertensive stress.
A single-center, observational cohort study assessing the mitochondrial bioenergetics of left ventricular tissue from patients undergoing coronary artery bypass grafting surgery suggests that viable myocardium has global alterations in bioenergetics and transcriptome without large regional differences between areas with or without inducible ischemia.