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  1. Article ; Online: Why is endothelial resilience key to maintain cardiac health?

    Tombor, Lukas S / Dimmeler, Stefanie

    Basic research in cardiology

    2022  Volume 117, Issue 1, Page(s) 35

    Abstract: Myocardial injury as induced by myocardial infarction results in tissue ischemia, which critically incepts cardiomyocyte death. Endothelial cells play a crucial role in restoring oxygen and nutrient supply to the heart. Latest advances in single-cell ... ...

    Abstract Myocardial injury as induced by myocardial infarction results in tissue ischemia, which critically incepts cardiomyocyte death. Endothelial cells play a crucial role in restoring oxygen and nutrient supply to the heart. Latest advances in single-cell multi-omics, together with genetic lineage tracing, reveal a transcriptional and phenotypical adaptation to the injured microenvironment, which includes alterations in metabolic, mesenchymal, hematopoietic and pro-inflammatory signatures. The extent of transition in mesenchymal or hematopoietic cell lineages is still debated, but it is clear that several of the adaptive phenotypical changes are transient and endothelial cells revert back to a naïve cell state after resolution of injury responses. This resilience of endothelial cells to acute stress responses is important for preventing chronic dysfunction. Here, we summarize how endothelial cells adjust to injury and how this dynamic response contributes to repair and regeneration. We will highlight intrinsic and microenvironmental factors that contribute to endothelial cell resilience and may be targetable to maintain a functionally active, healthy microcirculation.
    MeSH term(s) Endothelial Cells/metabolism ; Humans ; Myocardial Infarction/metabolism ; Myocytes, Cardiac/metabolism
    Language English
    Publishing date 2022-07-14
    Publishing country Germany
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 189755-x
    ISSN 1435-1803 ; 0300-8428 ; 0175-9418
    ISSN (online) 1435-1803
    ISSN 0300-8428 ; 0175-9418
    DOI 10.1007/s00395-022-00941-8
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  2. Article ; Online: Comparative analysis of common alignment tools for single-cell RNA sequencing.

    Brüning, Ralf Schulze / Tombor, Lukas / Schulz, Marcel H / Dimmeler, Stefanie / John, David

    GigaScience

    2022  Volume 11

    Abstract: Background: With the rise of single-cell RNA sequencing new bioinformatic tools have been developed to handle specific demands, such as quantifying unique molecular identifiers and correcting cell barcodes. Here, we benchmarked several datasets with the ...

    Abstract Background: With the rise of single-cell RNA sequencing new bioinformatic tools have been developed to handle specific demands, such as quantifying unique molecular identifiers and correcting cell barcodes. Here, we benchmarked several datasets with the most common alignment tools for single-cell RNA sequencing data. We evaluated differences in the whitelisting, gene quantification, overall performance, and potential variations in clustering or detection of differentially expressed genes. We compared the tools Cell Ranger version 6, STARsolo, Kallisto, Alevin, and Alevin-fry on 3 published datasets for human and mouse, sequenced with different versions of the 10X sequencing protocol.
    Results: Striking differences were observed in the overall runtime of the mappers. Besides that, Kallisto and Alevin showed variances in the number of valid cells and detected genes per cell. Kallisto reported the highest number of cells; however, we observed an overrepresentation of cells with low gene content and unknown cell type. Conversely, Alevin rarely reported such low-content cells. Further variations were detected in the set of expressed genes. While STARsolo, Cell Ranger 6, Alevin-fry, and Alevin produced similar gene sets, Kallisto detected additional genes from the Vmn and Olfr gene family, which are likely mapping artefacts. We also observed differences in the mitochondrial content of the resulting cells when comparing a prefiltered annotation set to the full annotation set that includes pseudogenes and other biotypes.
    Conclusion: Overall, this study provides a detailed comparison of common single-cell RNA sequencing mappers and shows their specific properties on 10X Genomics data.
    MeSH term(s) Animals ; Cluster Analysis ; Computational Biology/methods ; Genomics ; Mice ; RNA ; Sequence Analysis, RNA/methods ; Single-Cell Analysis ; Software
    Chemical Substances RNA (63231-63-0)
    Language English
    Publishing date 2022-04-04
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2708999-X
    ISSN 2047-217X ; 2047-217X
    ISSN (online) 2047-217X
    ISSN 2047-217X
    DOI 10.1093/gigascience/giac001
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  3. Article ; Online: Improved integration of single-cell transcriptome data demonstrates common and unique signatures of heart failure in mice and humans.

    Jurado, Mariano Ruz / Tombor, Lukas S / Arsalan, Mani / Holubec, Tomas / Emrich, Fabian / Walther, Thomas / Abplanalp, Wesley / Fischer, Ariane / Zeiher, Andreas M / Schulz, Marcel H / Dimmeler, Stefanie / John, David

    GigaScience

    2024  Volume 13

    Abstract: Background: Cardiovascular research heavily relies on mouse (Mus musculus) models to study disease mechanisms and to test novel biomarkers and medications. Yet, applying these results to patients remains a major challenge and often results in ... ...

    Abstract Background: Cardiovascular research heavily relies on mouse (Mus musculus) models to study disease mechanisms and to test novel biomarkers and medications. Yet, applying these results to patients remains a major challenge and often results in noneffective drugs. Therefore, it is an open challenge of translational science to develop models with high similarities and predictive value. This requires a comparison of disease models in mice with diseased tissue derived from humans.
    Results: To compare the transcriptional signatures at single-cell resolution, we implemented an integration pipeline called OrthoIntegrate, which uniquely assigns orthologs and therewith merges single-cell RNA sequencing (scRNA-seq) RNA of different species. The pipeline has been designed to be as easy to use and is fully integrable in the standard Seurat workflow.We applied OrthoIntegrate on scRNA-seq from cardiac tissue of heart failure patients with reduced ejection fraction (HFrEF) and scRNA-seq from the mice after chronic infarction, which is a commonly used mouse model to mimic HFrEF. We discovered shared and distinct regulatory pathways between human HFrEF patients and the corresponding mouse model. Overall, 54% of genes were commonly regulated, including major changes in cardiomyocyte energy metabolism. However, several regulatory pathways (e.g., angiogenesis) were specifically regulated in humans.
    Conclusions: The demonstration of unique pathways occurring in humans indicates limitations on the comparability between mice models and human HFrEF and shows that results from the mice model should be validated carefully. OrthoIntegrate is publicly accessible (https://github.com/MarianoRuzJurado/OrthoIntegrate) and can be used to integrate other large datasets to provide a general comparison of models with patient data.
    MeSH term(s) Humans ; Animals ; Mice ; Heart Failure/genetics ; Transcriptome ; Stroke Volume ; Energy Metabolism ; RNA
    Chemical Substances RNA (63231-63-0)
    Language English
    Publishing date 2024-02-07
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2708999-X
    ISSN 2047-217X ; 2047-217X
    ISSN (online) 2047-217X
    ISSN 2047-217X
    DOI 10.1093/gigascience/giae011
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  4. Article: Acute injury to the mouse carotid artery provokes a distinct healing response.

    Warwick, Timothy / Buchmann, Giulia Karolin / Pflüger-Müller, Beatrice / Spaeth, Manuela / Schürmann, Christoph / Abplanalp, Wesley / Tombor, Lukas / John, David / Weigert, Andreas / Leo-Hansmann, Martin / Dimmeler, Stefanie / Brandes, Ralf P

    Frontiers in physiology

    2023  Volume 14, Page(s) 1125864

    Abstract: Treatment of vascular stenosis with angioplasty results in acute vascular damage, which may lead to restenosis. Owing to the highly complex cellularity of blood vessels, the healing response following this damage is incompletely understood. To gain ... ...

    Abstract Treatment of vascular stenosis with angioplasty results in acute vascular damage, which may lead to restenosis. Owing to the highly complex cellularity of blood vessels, the healing response following this damage is incompletely understood. To gain further insight into this process, scRNA-seq of mouse carotid tissue after wire injury was performed. Stages of acute inflammation, resolution and remodeling were recapitulated in these data. To identify cell types which give rise to neointima, analyses focused on smooth muscle cell and fibroblast populations, and included data integration with scRNA-seq data from myocardial infarction and atherosclerosis datasets. Following carotid injury, a subpopulation of smooth muscle cells which also arises during atherosclerosis and myocardial infarction was identified. So-called stem cell/endothelial cell/monocyte (SEM) cells are candidates for repopulating injured vessels, and were amongst the most proliferative cell clusters following wire-injury of the carotid artery. Importantly, SEM cells exhibit specific transcriptional profiles which could be therapeutically targeted. SEM cell gene expression patterns could also be detected in bulk RNA-sequencing of neointimal tissue isolated from injured carotid vessels by laser capture microdissection. These data indicate that phenotypic plasticity of smooth muscle cells is highly important to the progression of lumen loss following acute carotid injury. Interference with SEM cell formation could be an innovative approach to combat development of restenosis.
    Language English
    Publishing date 2023-02-07
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2564217-0
    ISSN 1664-042X
    ISSN 1664-042X
    DOI 10.3389/fphys.2023.1125864
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  5. Article ; Online: Cardiomyocyte hyperplasia and immaturity but not hypertrophy are characteristic features of patients with RASopathies.

    Drenckhahn, Jörg-Detlef / Nicin, Luka / Akhouaji, Sara / Krück, Svenja / Blank, Anna Eva / Schänzer, Anne / Yörüker, Uygar / Jux, Christian / Tombor, Lukas / Abplanalp, Wesley / John, David / Zeiher, Andreas M / Dimmeler, Stefanie / Rupp, Stefan

    Journal of molecular and cellular cardiology

    2023  Volume 178, Page(s) 22–35

    Abstract: Aims: RASopathies are caused by mutations in genes that alter the MAP kinase pathway and are marked by several malformations with cardiovascular disorders as the predominant cause of mortality. Mechanistic insights in the underlying pathogenesis in ... ...

    Abstract Aims: RASopathies are caused by mutations in genes that alter the MAP kinase pathway and are marked by several malformations with cardiovascular disorders as the predominant cause of mortality. Mechanistic insights in the underlying pathogenesis in affected cardiac tissue are rare. The aim of the study was to assess the impact of RASopathy causing mutations on the human heart.
    Methods and results: Using single cell approaches and histopathology we analyzed cardiac tissue from children with different RASopathy-associated mutations compared to age-matched dilated cardiomyopathy (DCM) and control hearts. The volume of cardiomyocytes was reduced in RASopathy conditions compared to controls and DCM patients, and the estimated number of cardiomyocytes per heart was ∼4-10 times higher. Single nuclei RNA sequencing of a 13-year-old RASopathy patient (carrying a PTPN11 c.1528C > G mutation) revealed that myocardial cell composition and transcriptional patterns were similar to <1 year old DCM hearts. Additionally, immaturity of cardiomyocytes is shown by an increased MYH6/MYH7 expression ratio and reduced expression of genes associated with fatty acid metabolism. In the patient with the PTPN11 mutation activation of the MAP kinase pathway was not evident in cardiomyocytes, whereas increased phosphorylation of PDK1 and its downstream kinase Akt was detected.
    Conclusion: In conclusion, an immature cardiomyocyte differentiation status appears to be preserved in juvenile RASopathy patients. The increased mass of the heart in such patients is due to an increase in cardiomyocyte number (hyperplasia) but not an enlargement of individual cardiomyocytes (hypertrophy).
    MeSH term(s) Child ; Infant ; Humans ; Adolescent ; Myocytes, Cardiac/metabolism ; Hyperplasia/metabolism ; Mutation ; Mitogen-Activated Protein Kinases/metabolism ; Hypertrophy/metabolism ; Cardiomyopathy, Dilated/genetics ; Cardiomyopathy, Dilated/metabolism
    Chemical Substances Mitogen-Activated Protein Kinases (EC 2.7.11.24)
    Language English
    Publishing date 2023-03-21
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 80157-4
    ISSN 1095-8584 ; 0022-2828
    ISSN (online) 1095-8584
    ISSN 0022-2828
    DOI 10.1016/j.yjmcc.2023.03.003
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  6. Article ; Online: Age-Dependent RGS5 Loss in Pericytes Induces Cardiac Dysfunction and Fibrosis.

    Tamiato, Anita / Tombor, Lukas S / Fischer, Ariane / Muhly-Reinholz, Marion / Vanicek, Leah Rebecca / Toğru, Büşra Nur / Neitz, Jessica / Glaser, Simone Franziska / Merten, Maximilian / Rodriguez Morales, David / Kwon, Jeonghyeon / Klatt, Stephan / Schumacher, Bianca / Günther, Stefan / Abplanalp, Wesley T / John, David / Fleming, Ingrid / Wettschureck, Nina / Dimmeler, Stefanie /
    Luxán, Guillermo

    Circulation research

    2024  Volume 134, Issue 10, Page(s) 1240–1255

    Abstract: Background: Pericytes are capillary-associated mural cells involved in the maintenance and stability of the vascular network. Although aging is one of the main risk factors for cardiovascular disease, the consequences of aging on cardiac pericytes are ... ...

    Abstract Background: Pericytes are capillary-associated mural cells involved in the maintenance and stability of the vascular network. Although aging is one of the main risk factors for cardiovascular disease, the consequences of aging on cardiac pericytes are unknown.
    Methods: In this study, we have combined single-nucleus RNA sequencing and histological analysis to determine the effects of aging on cardiac pericytes. Furthermore, we have conducted in vivo and in vitro analysis of RGS5 (regulator of G-protein signaling 5) loss of function and finally have performed pericytes-fibroblasts coculture studies to understand the effect of RGS5 deletion in pericytes on the neighboring fibroblasts.
    Results: Aging reduced the pericyte area and capillary coverage in the murine heart. Single-nucleus RNA sequencing analysis further revealed that the expression of
    Conclusions: Our results have identified RGS5 as a crucial regulator of pericyte function during cardiac aging. The deletion of RGS5 causes cardiac dysfunction and induces myocardial fibrosis, one of the hallmarks of cardiac aging.
    MeSH term(s) Pericytes/metabolism ; Pericytes/pathology ; Animals ; RGS Proteins/genetics ; RGS Proteins/metabolism ; RGS Proteins/deficiency ; Fibrosis ; Fibroblasts/metabolism ; Fibroblasts/pathology ; Mice ; Cells, Cultured ; Aging/metabolism ; Aging/pathology ; Mice, Inbred C57BL ; Mice, Knockout ; Myocardium/metabolism ; Myocardium/pathology ; Male ; Coculture Techniques
    Chemical Substances RGS Proteins ; Rgs5 protein, mouse
    Language English
    Publishing date 2024-04-02
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 80100-8
    ISSN 1524-4571 ; 0009-7330 ; 0931-6876
    ISSN (online) 1524-4571
    ISSN 0009-7330 ; 0931-6876
    DOI 10.1161/CIRCRESAHA.123.324183
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  7. Article ; Online: Single-nuclear transcriptome profiling identifies persistent fibroblast activation in hypertrophic and failing human hearts of patients with longstanding disease.

    Kattih, Badder / Boeckling, Felicitas / Shumliakivska, Mariana / Tombor, Lukas / Rasper, Tina / Schmitz, Katja / Hoffmann, Jedrzej / Nicin, Luka / Abplanalp, Wesley T / Carstens, Daniel C / Arsalan, Mani / Emrich, Fabian / Holubec, Tomas / Walther, Thomas / Puntmann, Valentina O / Nagel, Eike / John, David / Zeiher, Andreas M / Dimmeler, Stefanie

    Cardiovascular research

    2023  Volume 119, Issue 15, Page(s) 2550–2562

    Abstract: Aims: Cardiac fibrosis drives the progression of heart failure in ischaemic and hypertrophic cardiomyopathy. Therefore, the development of specific anti-fibrotic treatment regimens to counteract cardiac fibrosis is of high clinical relevance. Hence, ... ...

    Abstract Aims: Cardiac fibrosis drives the progression of heart failure in ischaemic and hypertrophic cardiomyopathy. Therefore, the development of specific anti-fibrotic treatment regimens to counteract cardiac fibrosis is of high clinical relevance. Hence, this study examined the presence of persistent fibroblast activation during longstanding human heart disease at a single-cell resolution to identify putative therapeutic targets to counteract pathological cardiac fibrosis in patients.
    Methods and results: We used single-nuclei RNA sequencing with human tissues from two samples of one healthy donor, and five hypertrophic and two failing hearts. Unsupervised sub-clustering of 7110 nuclei led to the identification of 7 distinct fibroblast clusters. De-convolution of cardiac fibroblast heterogeneity revealed a distinct population of human cardiac fibroblasts with a molecular signature of persistent fibroblast activation and a transcriptional switch towards a pro-fibrotic extra-cellular matrix composition in patients with established cardiac hypertrophy and heart failure. This sub-cluster was characterized by high expression of POSTN, RUNX1, CILP, and a target gene adipocyte enhancer-binding protein 1 (AEBP1) (all P < 0.001). Strikingly, elevated circulating AEBP1 blood level were also detected in a validation cohort of patients with confirmed cardiac fibrosis and hypertrophic cardiomyopathy by cardiac magnetic resonance imaging (P < 0.01). Since endogenous AEBP1 expression was increased in patients with established cardiac hypertrophy and heart failure, we assessed the functional consequence of siRNA-mediated AEBP1 silencing in human cardiac fibroblasts. Indeed, AEBP1 silencing reduced proliferation, migration, and fibroblast contractile capacity and α-SMA gene expression, which is a hallmark of fibroblast activation (all P < 0.05). Mechanistically, the anti-fibrotic effects of AEBP1 silencing were linked to transforming growth factor-beta pathway modulation.
    Conclusion: Together, this study identifies persistent fibroblast activation in patients with longstanding heart disease, which might be detected by circulating AEBP1 and therapeutically modulated by its targeted silencing in human cardiac fibroblasts.
    MeSH term(s) Humans ; Heart Failure/metabolism ; Heart Diseases/pathology ; Cardiomegaly/metabolism ; Cardiomyopathy, Hypertrophic/metabolism ; Cardiomyopathies/metabolism ; Fibrosis ; Fibroblasts/metabolism ; Gene Expression Profiling ; Carboxypeptidases/metabolism ; Repressor Proteins/metabolism
    Chemical Substances AEBP1 protein, human ; Carboxypeptidases (EC 3.4.-) ; Repressor Proteins
    Language English
    Publishing date 2023-08-30
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 80340-6
    ISSN 1755-3245 ; 0008-6363
    ISSN (online) 1755-3245
    ISSN 0008-6363
    DOI 10.1093/cvr/cvad140
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  8. Article ; Online: The hydrogen-peroxide producing NADPH oxidase 4 does not limit neointima development after vascular injury in mice.

    Buchmann, Giulia K / Schürmann, Christoph / Spaeth, Manuela / Abplanalp, Wesley / Tombor, Lukas / John, David / Warwick, Timothy / Rezende, Flávia / Weigert, Andreas / Shah, Ajay M / Hansmann, Martin-Leo / Weissmann, Norbert / Dimmeler, Stefanie / Schröder, Katrin / Brandes, Ralf P

    Redox biology

    2021  Volume 45, Page(s) 102050

    Abstract: Objective: The NADPH oxidase Nox4 is an important source of H: Methods and results: Genetic deletion of Nox4 by a tamoxifen-activated Cre-Lox-system did not impact on neointima formation in the carotid artery wire injury model. To understand this ... ...

    Abstract Objective: The NADPH oxidase Nox4 is an important source of H
    Methods and results: Genetic deletion of Nox4 by a tamoxifen-activated Cre-Lox-system did not impact on neointima formation in the carotid artery wire injury model. To understand this unexpected finding, time-resolved single-cell RNA-sequencing (scRNAseq) from injured carotid arteries of control mice and massive-analysis-of-cDNA-ends (MACE)-RNAseq from the neointima harvested by laser capture microdissection of control and Nox4 knockout mice was performed. This revealed that resting smooth muscle cells (SMCs) and fibroblasts exhibit high Nox4 expression, but that the proliferating de-differentiated SMCs, which give rise to the neointima, have low Nox4 expression. In line with this, the first weeks after injury, gene expression was unchanged between the carotid artery neointimas of control and Nox4 knockout mice.
    Conclusion: Upon vascular injury, Nox4 expression is transiently lost in the cells which comprise the neointima. NADPH oxidase 4 therefore does not interfere with restenosis development after wire-induced vascular injury.
    MeSH term(s) Animals ; Cells, Cultured ; Hydrogen Peroxide ; Mice ; Mice, Knockout ; Myocytes, Smooth Muscle ; NADPH Oxidase 4/genetics ; Neointima ; Vascular System Injuries
    Chemical Substances Hydrogen Peroxide (BBX060AN9V) ; NADPH Oxidase 4 (EC 1.6.3.-) ; Nox4 protein, mouse (EC 1.6.3.-)
    Language English
    Publishing date 2021-06-18
    Publishing country Netherlands
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2701011-9
    ISSN 2213-2317 ; 2213-2317
    ISSN (online) 2213-2317
    ISSN 2213-2317
    DOI 10.1016/j.redox.2021.102050
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  9. Article ; Online: Cell type-specific expression of the putative SARS-CoV-2 receptor ACE2 in human hearts.

    Nicin, Luka / Abplanalp, Wesley Tyler / Mellentin, Hannah / Kattih, Badder / Tombor, Lukas / John, David / Schmitto, Jan D / Heineke, Jörg / Emrich, Fabian / Arsalan, Mani / Holubec, Tomas / Walther, Thomas / Zeiher, Andreas M / Dimmeler, Stefanie

    European heart journal

    2020  Volume 41, Issue 19, Page(s) 1804–1806

    MeSH term(s) Aged ; Aged, 80 and over ; Angiotensin-Converting Enzyme 2 ; Betacoronavirus ; COVID-19 ; Case-Control Studies ; Cell Nucleus/genetics ; Coronavirus Infections ; Female ; Gene Expression ; Humans ; Male ; Middle Aged ; Myocardium/cytology ; Myocytes, Cardiac/metabolism ; Pandemics ; Peptidyl-Dipeptidase A/genetics ; Peptidyl-Dipeptidase A/metabolism ; Pneumonia, Viral ; SARS-CoV-2 ; Sequence Analysis, RNA
    Chemical Substances ACE protein, human (EC 3.4.15.1) ; Peptidyl-Dipeptidase A (EC 3.4.15.1) ; ACE2 protein, human (EC 3.4.17.23) ; Angiotensin-Converting Enzyme 2 (EC 3.4.17.23)
    Keywords covid19
    Language English
    Publishing date 2020-04-15
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 603098-1
    ISSN 1522-9645 ; 0195-668X
    ISSN (online) 1522-9645
    ISSN 0195-668X
    DOI 10.1093/eurheartj/ehaa311
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  10. Article ; Online: Single Nuclei Sequencing Reveals Novel Insights Into the Regulation of Cellular Signatures in Children With Dilated Cardiomyopathy.

    Nicin, Luka / Abplanalp, Wesley T / Schänzer, Anne / Sprengel, Anke / John, David / Mellentin, Hannah / Tombor, Lukas / Keuper, Matthias / Ullrich, Evelyn / Klingel, Karin / Dettmeyer, Reinhard B / Hoffmann, Jedrzej / Akintuerk, Hakan / Jux, Christian / Schranz, Dietmar / Zeiher, Andreas M / Rupp, Stefan / Dimmeler, Stefanie

    Circulation

    2021  Volume 143, Issue 17, Page(s) 1704–1719

    Abstract: Background: Dilated cardiomyopathy (DCM) is a leading cause of death in children with heart failure. The outcome of pediatric heart failure treatment is inconsistent, and large cohort studies are lacking. Progress may be achieved through personalized ... ...

    Abstract Background: Dilated cardiomyopathy (DCM) is a leading cause of death in children with heart failure. The outcome of pediatric heart failure treatment is inconsistent, and large cohort studies are lacking. Progress may be achieved through personalized therapy that takes age- and disease-related pathophysiology, pathology, and molecular fingerprints into account. We present single nuclei RNA sequencing from pediatric patients with DCM as the next step in identifying cellular signatures.
    Methods: We performed single nuclei RNA sequencing with heart tissues from 6 children with DCM with an age of 0.5, 0.75, 5, 6, 12, and 13 years. Unsupervised clustering of 18 211 nuclei led to the identification of 14 distinct clusters with 6 major cell types.
    Results: The number of nuclei in fibroblast clusters increased with age in patients with DCM, a finding that was confirmed by histological analysis and was consistent with an age-related increase in cardiac fibrosis quantified by cardiac magnetic resonance imaging. Fibroblasts of patients with DCM >6 years of age showed a profoundly altered gene expression pattern with enrichment of genes encoding fibrillary collagens, modulation of proteoglycans, switch in thrombospondin isoforms, and signatures of fibroblast activation. In addition, a population of cardiomyocytes with a high proregenerative profile was identified in infant patients with DCM but was absent in children >6 years of age. This cluster showed high expression of cell cycle activators such as
    Conclusions: Novel insights into the cellular transcriptomes of hearts from pediatric patients with DCM provide remarkable age-dependent changes in the expression patterns of fibroblast and cardiomyocyte genes with less fibrotic but enriched proregenerative signatures in infants.
    MeSH term(s) Cardiomyopathy, Dilated/genetics ; Cardiomyopathy, Dilated/pathology ; Cell Proliferation ; Child ; Child, Preschool ; Female ; High-Throughput Nucleotide Sequencing/methods ; Humans ; Male ; Sequence Analysis, RNA/methods
    Language English
    Publishing date 2021-02-23
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 80099-5
    ISSN 1524-4539 ; 0009-7322 ; 0069-4193 ; 0065-8499
    ISSN (online) 1524-4539
    ISSN 0009-7322 ; 0069-4193 ; 0065-8499
    DOI 10.1161/CIRCULATIONAHA.120.051391
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