{'fraction_non_alphanumeric': 0.026465028355387523, 'fraction_numerical': 0.005198487712665407, 'mean_word_length': 5.829032258064516, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Making muscle: overview to "Cardiovascular lineage commitment during development and regeneration" series.

Those unnerved by the evolutionary relatedness between humans and chimpanzees might do well to consider the humble brewer' s yeast, Saccharomyces cerevisiae, and fission yeast, S pombe.1 At the biochemical level, we three are so similar that human orthologs can correct lethal defects of the corresponding yeast genes.2,3 Apart from merely single genes, this conservation extends to entire networks (eg, signal transduction by a web of protein kinases), modules (eg, cell cycle regulators), and multimolecular machines (eg, the telosome). For these reasons, although a stretch at first glance, yeast provide extraordinary insights into many underpinnings of cardiovascular medicine, shaping the course of research on cardiac muscle cell growth, proliferation, and aging.4,5

However, for multicellular life, assembling the organism gives rise to a further job description: creating the right cell type, in precisely the right place, at the right time. Understanding this set of decisions and the responsible molecular circuits is a prerequisite if one is to appreciate the multiple ways in which developmental biology permeates cardiovascular medicine and to draw on this knowledge for translational benefits.6 The impact of cardiovascular development is most obvious with regard to congenital heart defects, often entailing mutations in heart-forming transcription factors and morphogens.7 Many of the same transcription factors are engaged in adult cardiac hypertrophy and heart failure, as mediators of the “fetal phenotype” triggered by workload, reprogramming the adult cardiomyocyte's mechanical performance, energetics, and susceptibility to death.8 A third context is potentially even more transformative therapeutically: taking the insights gleaned from heart muscle formation by model organisms and multipotent stem cells and then applying them to the daunting but irresistible task of enhancing human heart regeneration.9,–,13

The present series of review articles for Circulation Research will …