Cardiovascular diseases articles from across Nature Portfolio

Genome-wide association studies (GWAS) in coronary artery disease have revealed gene variants highly expressed in vascular smooth muscles cells (SMCs). Research now suggests that loss of one, Prdm16, drives a switch toward a synthetic SMC phenotype, with robust, potentially protective extracellular matrix production and fibrous cap formation.

Dilated cardiomyopathy (DCM) is more prevalent among individuals of African descent, but a genetic basis for this increased risk has remained unclear. By integrating genomic and phenotypic data from multiple African ancestry cohorts, we identified a common, ancestry-specific nonsense variant in CD36 that increases DCM risk by impairing myocardial energetics. This variant explains one-fifth of the excess DCM burden observed in individuals of African descent.

The first-in-human trial of AAV2i8-I1c (AB-1002) — an adeno-associated virus vector that targets a protein phosphatase inhibitor to cardiac muscle — suggests a cautious return of cardiac gene therapy after earlier setbacks, with a new target, dose optimization and improved vector design shaping future directions.

Psychological stress is linked to poor cardiovascular outcomes, but its risk impact may vary with age. Here, the authors show that stress-related brain activity predicts mortality, especially in younger adults, while its influence weakens with age and comorbidities.

Genome-wide association studies (GWAS) in coronary artery disease have revealed gene variants highly expressed in vascular smooth muscles cells (SMCs). Research now suggests that loss of one, Prdm16, drives a switch toward a synthetic SMC phenotype, with robust, potentially protective extracellular matrix production and fibrous cap formation.

Shafqat Ahmad and Gull Rukh discuss a landmark, twin-based, epidemiological study that highlighted how genetic predisposition and environmental factors interact to influence the risk of coronary heart disease.

Valtteri Muroke discusses the LoDoCo trial, in which treatment with low-dose colchicine was shown to reduce cardiovascular end points in patients with stable coronary artery disease, identifying anti-inflammatory therapy as an effective strategy for the secondary prevention of cardiovascular events.

Dilated cardiomyopathy (DCM) is more prevalent among individuals of African descent, but a genetic basis for this increased risk has remained unclear. By integrating genomic and phenotypic data from multiple African ancestry cohorts, we identified a common, ancestry-specific nonsense variant in CD36 that increases DCM risk by impairing myocardial energetics. This variant explains one-fifth of the excess DCM burden observed in individuals of African descent.