Lhoste et al. show that cardiometabolic and renal traits of the US population have shifted from phenotypes with high blood pressure and high cholesterol toward poor kidney function, hyperglycemia and severe obesity.

Selvakumar, Clayton et al. use a porcine model of myocardial infarction and PSC-CM transplantation and identify atrial and pacemaker-like cardiomyocytes as the cause of engraftment arrhythmias and surface marker signatures to distinguish between arrhythmogenic and non-arrhythmogenic cardiomyocytes.

Goerlich et al. review the current knowledge of the cardiovascular complications of the post-COVID condition, including postural orthostatic tachycardia syndrome, myocardial injury, heart failure, myocarditis and arrhythmias, highlighting currently available and potential treatments.

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.

Hu et al. describe how histone H1.0 regulates myofibroblast activation, linking force generation to nuclear organization and gene transcription.

In a retrospective cohort study examining the comparative effectiveness of diabetes drugs in adults at moderate risk for cardiovascular disease, GLP-1 receptor agonists and SGLT2 inhibitors reduced the risk of cardiovascular events compared to DPP4 inhibitors, whereas sulfonylureas increased the risk.

Antila et al. show that brain amyloid-β load is not significantly affected by sustained dural lymphatic vessel atrophy or hyperplasia induced by lymphangiogenic growth factor manipulation in two mouse models of Alzheimer’s disease.

Brash et al. created the BulkECexplorer, an online tool based on 240 endothelial bulk RNA-seq datasets, which predicts active or leaky gene expression in five vascular endothelial cell subtypes.

Piollet, Porsch et al. report that the myeloid receptor TREM2 limits necrotic core formation in atherosclerosis and controls key atherosclerosis-related functions of macrophages, such as efferocytosis, lipid uptake and foam cell survival.

Using two complementary approaches to induce hypercholesterolemia in mice, Di Nunzio, Hellberg, Zhang, Ahmed et al. identified liver macrophages as key cells that organize the systemic responses to lipoproteins during the initial phases of atherosclerosis pathogenesis.

Although anti-inflammatory drugs have shown promising results in preclinical cardiovascular research, they have yielded little benefit in clinical trials. Before we can expect positive outcomes, we need to find ways of stratifying patients based on their infectious, inflammatory and autoimmune profile, and identify the right time of treatment.