Single-cell multiomics and chromatin structure reveal gene-regulatory dynamics in heart failure.
Y, X., L, T., EN, F., L, C., Q, Y., TS, S., W, E., S, T., J, D., & A, L. (2026). Single-cell multiomics and chromatin structure reveal gene-regulatory dynamics in heart failure.. Science (New York, N.Y.). https://doi.org/10.1126/science.ady6893
Y X, L T, EN F, L C, Q Y, TS S, et al. Single-cell multiomics and chromatin structure reveal gene-regulatory dynamics in heart failure.. Science (New York, N.Y.). 2026; doi: 10.1126/science.ady6893
Y X, L T, EN F, et al. Single-cell multiomics and chromatin structure reveal gene-regulatory dynamics in heart failure.[J]. Science (New York, N.Y.). 2026. DOI: 10.1126/science.ady6893.
@article{y2026,
author = {Xie Y and Tucciarone L and Farah EN and Chang L and Yang Q and Shankar TS and Elison W and Tran S and Djulamsah J and Lie A},
title = {Single-cell multiomics and chromatin structure reveal gene-regulatory dynamics in heart failure.},
journal = {Science (New York, N.Y.)},
year = {2026},
doi = {10.1126/science.ady6893},
note = {PMID: 42490484},
}
TY - JOUR AU - Xie Y AU - Tucciarone L AU - Farah EN AU - Chang L AU - Yang Q AU - Shankar TS AU - Elison W AU - Tran S AU - Djulamsah J AU - Lie A TI - Single-cell multiomics and chromatin structure reveal gene-regulatory dynamics in heart failure. T2 - Science (New York, N.Y.) PY - 2026 DO - 10.1126/science.ady6893 AN - PMID:42490484 ER -
Heart failure is a leading cause of morbidity and mortality, yet gene-regulatory mechanisms driving cell type-specific pathologic responses remain undefined. Here, we present the cell type-resolved transcriptomes, chromatin accessibility, histone modifications, and chromatin organization of 13 nonfailing and 23 failing human hearts across all cardiac chambers. Integrative analyses revealed dynamic changes in cell type composition, gene-regulatory programs, and chromatin organization, particularly in cardiomyocytes and fibroblasts. Mapping cell type-specific enhancer-gene interactions from these analyses enabled the illumination of likely causal genetic contributors to heart failure from genetic association data. Together, these findings provide multimodal gene-regulatory maps of the human heart in health and disease, offering a framework for designing precise, cell type-targeted therapies for treating heart failure.