Multiomic Spatial Mapping of Myocardial Infarction and Implications for Personalized Therapy

David Schumacher, Rafael Kramann*

*Corresponding author for this work

Research output: Contribution to journalReview articleAcademicpeer-review

8 Citations (Scopus)
19 Downloads (Pure)

Abstract

Ischemic heart disease including myocardial infarction is still the leading cause of death worldwide. Although the survival early after myocardial infarction has been significantly improved by the introduction of percutaneous coronary intervention, long-term morbidity and mortality remain high. The elevated long-term mortality is mainly driven by cardiac remodeling processes triggering ischemic heart failure and electric instability. Despite the new developments in pharmaco-therapy of heart failure, we still lack targeted therapies for cardiac remodeling and fibrosis. Single-cell and genomic technologies allow us to map the human heart at unprecedented resolution and allow to gain insights into cellular and molecular heterogeneity. However, these technologies rely on digested tissue and isolated cells or nuclei and thus lack spatial information. Spatial information is critical to understand tissue homeostasis and disease and can be utilized to identify disease-driving cell populations and mechanisms including cellular cross-talk. Here, we discuss recent advances in single-cell and spatial genomic technologies that give insights into cellular and molecular mechanisms of cardiac remodeling after injury and can be utilized to identify novel therapeutic targets and pave the way toward new therapies in heart failure.

Original languageEnglish
Pages (from-to)192-202
Number of pages11
JournalArteriosclerosis, Thrombosis, and Vascular Biology
Volume43
Issue number2
DOIs
Publication statusPublished - Feb 2023

Bibliographical note

Funding Information:
This work was supported by the Clinician Scientist program of the Faculty of Medicine of the RWTH (Rheinisch-Westfälische Technische Hochschule) Aachen University (to D. Schumacher). This work was further supported by grants of the German Research Foundation (DFG: SFBTRR219 322900939, CRU344- 4288578857858 CRU5011- 445703531), a grant of the Else Kroener Fresenius Foundation (EKFS), the Dutch Kidney Foundation (DKF), TASKFORCE EP1805 and by the BMBF (Bundesministerium für Bildung und Forschung) eMed Consortia Fibromap and the ERA-CVD (European Research Area Network on Cardiovascular Diseases) MENDAGE (Dissecting Mesenchymal-Endothelial Cross-Talk, Heterogeneity and Function to Mend Vascular Ageing and Atherosclerosis) consortium (BMBF 01KL1907), the now (Nederlandse Organisatie voor Wetenschappelijk Onderzoek) Vidi 09150172010072 and the Leducq Foundation transatlantic network of excellence ImmunoFibHF all to R. Kramann.

Publisher Copyright:
© 2023 American Heart Association, Inc.

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