Heart development articles from across Nature Portfolio

The genetic link between placenta function and congenital heart defects has been established, though the cellular mechanisms underlying this connection is less clear. Here they show that PIBF1 regulates syncytiotrophoblast fusion and that loss of PIBF1 also negatively impacts heart development, providing a potential link between the development of these two organs.

Pluripotent stem cell-derived organoids can recapitulate significant hallmarks of human organ development and are becoming critical tools for human research. Here, the authors report significant technical steps for generating sophisticated synthetic human primitive heart organoids.

Catecholaminergic transmitters are critical signalling effectors known to be released by sympathetic nerves and adrenomedullary endocrine cells in response to physiological stress. In this paper, the authors demonstrate a uniquely distributed group of catecholaminergic cardiomyocytes with key regulatory roles in cardiac excitation conduction.

In a study published in Nature, Jia and colleagues use advanced optical electrophysiology tools coupled with 3D-printed moulds to capture the very first heartbeat of zebrafish.

Several experimental systems have been used over the past five decades to address important questions in cardiac development and congenital heart disease. Here we discuss the strengths and limitations of available models, and how the use of different models synergistically is needed for a deeper understanding of these complex diseases.

The essential omega-6 polyunsaturated fatty acid γ-linolenic acid present in maternal milk coordinates cardiac adaptation and survival in newborn mice, according to a new study.

The epicardium has an active role in the formation of fetal and neonatal mammalian hearts, which retain the ability to regenerate. A single-cell comparison of human fetal and adult epicardial cells defines the transcriptomic programs that are specific to the fetal epicardium that could be harnessed to repair the injured adult heart.

Cardiac sex-specific differences are controlled not only by sex hormones but also through a sex-chromosome-dependent mechanism. A new study in mice shows that cardiac sex-specific disparities appear at early stages of heart development, before gonad formation, and that X-linked genes act outside of the gonads in a dosage-dependent mechanism to regulate male–female cardiac differences.

A new study published in Cell shows that cardiac mesoderm has the capacity to self-organize and form into chamber-like structures known as cardioids.