ArticleCell death discovery2023
Dynamic chromatin landscape encodes programs for perinatal transition of cardiomyocytes.
Article in Cell death discovery, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 3 citations in OpenAlex.
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- Frameshift variants in C10orf71 cause dilated cardiomyopathy in human, mouse, and organoid models.The Journal of clinical investigation · 2024Article
- Thrombospondin 1 and Reelin act through Vldlr to regulate cardiac growth and repair.Basic research in cardiology · 2024Article
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Corrections and comments
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Authors and funding
11 authors at 5 institutions in 1 country.
Funding
Abstract
The perinatal period occurring immediately before and after birth is critical for cardiomyocytes because they must change rapidly to accommodate the switch from fetal to neonatal circulation after birth. This transition is a well-orchestrated process, and any perturbation leads to unhealthy cardiomyocytes and heart disease. Despite its importance, little is known about how this transition is regulated and controlled. Here, by mapping the genome-wide chromatin accessibility, transcription-centered long-range chromatin interactions and gene expression in cardiomyocytes undergoing perinatal transition, we discovered two key transcription factors, MEF2 and AP1, that are crucial for driving the phenotypic changes within the perinatal window. Thousands of dynamic regulatory elements were found in perinatal cardiomyocytes and we show these elements mediated the transcriptional reprogramming through an elegant chromatin high-order architecture. We recompiled transcriptional program of induced stem cell-derived cardiomyocytes according to our discovered network, and they showed adult cardiomyocyte-like electrophysiological expression. Our work provides a comprehensive regulatory resource of cardiomyocytes perinatal reprogramming, and aids the gap-filling of cardiac translational research.
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Registered trials
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