A1 Refereed original research article in a scientific journal
Transcriptomic and spatial dissection of human ex vivo right atrial tissue reveals proinflammatory microvascular changes in ischemic heart disease
Authors: Linna-Kuosmanen Suvi, Schmauch Eloi, Galani Kyriakitsa, Ojanen Johannes, Boix Carles A., Örd Tiit, Toropainen Anu, Singha Prosanta K., Moreau Pierre R., Harju Kristiina, Blazeski Adriana, Segerstolpe Åsa, Lahtinen Veikko, Hou Lei, Kang Kai, Meibalan Elamaran, Agudelo Leandro Z., Kokki Hannu, Halonen Jari, Jalkanen Juho, Gunn Jarmo, MacRae Calum A., Hollmén Maija, Hartikainen Juha E.K., Kaikkonen Minna U., García-Cardeña Guillermo, Tavi Pasi, Kiviniemi Tuomas, Kellis Manolis
Publisher: Cell Press
Publication year: 2024
Journal: Cell Reports Medicine
Journal name in source: Cell Reports Medicine
Article number: 101556
Volume: 5
Issue: 5
ISSN: 2666-3791
eISSN: 2666-3791
DOI: https://doi.org/10.1016/j.xcrm.2024.101556
Web address : https://doi.org/10.1016/j.xcrm.2024.101556
Self-archived copy’s web address: https://research.utu.fi/converis/portal/detail/Publication/421361402
Cardiovascular disease plays a central role in the electrical and structural remodeling of the right atrium, predisposing to arrhythmias, heart failure, and sudden death. Here, we dissect with single-nuclei RNA sequencing (snRNA-seq) and spatial transcriptomics the gene expression changes in the human ex vivo right atrial tissue and pericardial fluid in ischemic heart disease, myocardial infarction, and ischemic and non-ischemic heart failure using asymptomatic patients with valvular disease who undergo preventive surgery as the control group. We reveal substantial differences in disease-associated gene expression in all cell types, collectively suggesting inflammatory microvascular dysfunction and changes in the right atrial tissue composition as the valvular and vascular diseases progress into heart failure. The data collectively suggest that investigation of human cardiovascular disease should expand to all functionally important parts of the heart, which may help us to identify mechanisms promoting more severe types of the disease.
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Funding information in the publication:
This work was supported by The Academy of Finland grants 342074 (S.L.K.), 333021 (M.U.K.),325510 (P.T.); Clinical Research Fund (EVO) of Turku University Hospital, Turku, Finland (T.K.); European Research Council (ERC) grant 802825 (M.U.K.); Finnish Association of Cardiothoracic Surgery (K.H.); Finnish Cardiac Society (K.H.); Finnish Foundation for Cardiovascular Research (S.L.K., P.R.M., M.U.K., P.T., and T.K.); Finnish Government Research Funding (K.H.); Finnish Medical Foundation (T.K.); Ida Montin Foundation (P.R.M.); Instrumentarium Science Foundation (P.R.M.); Saastamoinen Foundation (E.S.); Sigrid Jusélius Foundation (S.L.K., M.U.K., and P.T.); Orion Research Foundation (S.L.K., E.S., and K.H.); and Yrjö Jahnsson Foundation (S.L.K. and E.S.). This work was supported in part by NIH grants AG081017, NS129032, NS115064, AG074003, NS127187, AG067151, and HG008155 (M.K.)
