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Article ; Online: The vasculature: a therapeutic target in heart failure?

Luxán, Guillermo / Dimmeler, Stefanie

2021 Volume 118, Issue 1, Page(s) 53–64

Abstract: It is well established that the vasculature plays a crucial role in maintaining oxygen and nutrients supply to the heart. Increasing evidence further suggests that the microcirculation has additional roles in supporting a healthy microenvironment. Heart ... ...

Abstract	It is well established that the vasculature plays a crucial role in maintaining oxygen and nutrients supply to the heart. Increasing evidence further suggests that the microcirculation has additional roles in supporting a healthy microenvironment. Heart failure is well known to be associated with changes and functional impairment of the microvasculature. The specific ablation of protective signals in endothelial cells in experimental models is sufficient to induce heart failure. Therefore, restoring a healthy endothelium and microcirculation may be a valuable therapeutic strategy to treat heart failure. This review article will summarize the current understanding of the vascular contribution to heart failure with reduced or preserved ejection fraction. Novel therapeutic approaches including next generation pro-angiogenic therapies and non-coding RNA therapeutics, as well as the targeting of metabolites or metabolic signalling, vascular inflammation and senescence will be discussed.
MeSH term(s)	Angiogenesis Inducing Agents/adverse effects ; Angiogenesis Inducing Agents/therapeutic use ; Animals ; Coronary Circulation/drug effects ; Coronary Vessels/drug effects ; Coronary Vessels/metabolism ; Coronary Vessels/physiopathology ; Genetic Therapy/adverse effects ; Heart Failure, Diastolic/genetics ; Heart Failure, Diastolic/metabolism ; Heart Failure, Diastolic/physiopathology ; Heart Failure, Diastolic/therapy ; Heart Failure, Systolic/genetics ; Heart Failure, Systolic/metabolism ; Heart Failure, Systolic/physiopathology ; Heart Failure, Systolic/therapy ; Humans ; Microcirculation/drug effects ; Microvessels/drug effects ; Microvessels/metabolism ; Microvessels/physiopathology ; Neovascularization, Physiologic/drug effects ; RNA, Untranslated/genetics ; RNA, Untranslated/metabolism ; Recovery of Function ; Vaccines/adverse effects ; Vaccines/therapeutic use ; Ventricular Function, Left/drug effects
Chemical Substances	Angiogenesis Inducing Agents ; RNA, Untranslated ; Vaccines
Language	English
Publishing date	2021-02-23
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	80340-6
ISSN	1755-3245 ; 0008-6363
ISSN (online)	1755-3245
ISSN	0008-6363
DOI	10.1093/cvr/cvab047
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Article: Fibroblast‐mediated intercellular crosstalk in the healthy and diseased heart

Nicin, Luka / Wagner, Julian U. G. / Luxán, Guillermo / Dimmeler, Stefanie

FEBS letters. 2022 Mar., v. 596, no. 5

2022

Abstract: Cardiac fibroblasts constitute a major cell population in the heart. They secrete extracellular matrix components and various other factors shaping the microenvironment of the heart. In silico analysis of intercellular communication based on single‐cell ... ...

Abstract	Cardiac fibroblasts constitute a major cell population in the heart. They secrete extracellular matrix components and various other factors shaping the microenvironment of the heart. In silico analysis of intercellular communication based on single‐cell RNA sequencing revealed that fibroblasts are the source of the majority of outgoing signals to other cell types. This observation suggests that fibroblasts play key roles in orchestrating cellular interactions that maintain organ homeostasis but that can also contribute to disease states. Here, we will review the current knowledge of fibroblast interactions in the healthy, diseased, and aging heart. We focus on the interactions that fibroblasts establish with other cells of the heart, specifically cardiomyocytes, endothelial cells and immune cells, and particularly those relying on paracrine, electrical, and exosomal communication modes.
Keywords	RNA ; cardiomyocytes ; cell communication ; computer simulation ; extracellular matrix ; fibroblasts ; homeostasis
Language	English
Dates of publication	2022-03
Size	p. 638-654.
Publishing place	John Wiley & Sons, Ltd
Document type	Article
Note	REVIEW
ZDB-ID	212746-5
ISSN	1873-3468 ; 0014-5793
ISSN (online)	1873-3468
ISSN	0014-5793
DOI	10.1002/1873-3468.14234
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Fibroblast-mediated intercellular crosstalk in the healthy and diseased heart.

Nicin, Luka / Wagner, Julian U G / Luxán, Guillermo / Dimmeler, Stefanie

FEBS letters

2021 Volume 596, Issue 5, Page(s) 638–654

Abstract	Cardiac fibroblasts constitute a major cell population in the heart. They secrete extracellular matrix components and various other factors shaping the microenvironment of the heart. In silico analysis of intercellular communication based on single-cell RNA sequencing revealed that fibroblasts are the source of the majority of outgoing signals to other cell types. This observation suggests that fibroblasts play key roles in orchestrating cellular interactions that maintain organ homeostasis but that can also contribute to disease states. Here, we will review the current knowledge of fibroblast interactions in the healthy, diseased, and aging heart. We focus on the interactions that fibroblasts establish with other cells of the heart, specifically cardiomyocytes, endothelial cells and immune cells, and particularly those relying on paracrine, electrical, and exosomal communication modes.
MeSH term(s)	Cell Communication ; Endothelial Cells ; Fibroblasts/metabolism ; Myocytes, Cardiac/metabolism
Language	English
Publishing date	2021-12-01
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	212746-5
ISSN	1873-3468 ; 0014-5793
ISSN (online)	1873-3468
ISSN	0014-5793
DOI	10.1002/1873-3468.14234
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Article ; Online: Malat1 deficiency prevents neonatal heart regeneration by inducing cardiomyocyte binucleation.

Aslan, Galip S / Jaé, Nicolas / Manavski, Yosif / Fouani, Youssef / Shumliakivska, Mariana / Kettenhausen, Lisa / Kirchhof, Luisa / Günther, Stefan / Fischer, Ariane / Luxán, Guillermo / Dimmeler, Stefanie

JCI insight

2023 Volume 8, Issue 5

Abstract: The adult mammalian heart has limited regenerative capacity, while the neonatal heart fully regenerates during the first week of life. Postnatal regeneration is mainly driven by proliferation of preexisting cardiomyocytes and supported by proregenerative ...

Abstract	The adult mammalian heart has limited regenerative capacity, while the neonatal heart fully regenerates during the first week of life. Postnatal regeneration is mainly driven by proliferation of preexisting cardiomyocytes and supported by proregenerative macrophages and angiogenesis. Although the process of regeneration has been well studied in the neonatal mouse, the molecular mechanisms that define the switch between regenerative and nonregenerative cardiomyocytes are not well understood. Here, using in vivo and in vitro approaches, we identified the lncRNA Malat1 as a key player in postnatal cardiac regeneration. Malat1 deletion prevented heart regeneration in mice after myocardial infarction on postnatal day 3 associated with a decline in cardiomyocyte proliferation and reparative angiogenesis. Interestingly, Malat1 deficiency increased cardiomyocyte binucleation even in the absence of cardiac injury. Cardiomyocyte-specific deletion of Malat1 was sufficient to block regeneration, supporting a critical role of Malat1 in regulating cardiomyocyte proliferation and binucleation, a landmark of mature nonregenerative cardiomyocytes. In vitro, Malat1 deficiency induced binucleation and the expression of a maturation gene program. Finally, the loss of hnRNP U, an interaction partner of Malat1, induced similar features in vitro, suggesting that Malat1 regulates cardiomyocyte proliferation and binucleation by hnRNP U to control the regenerative window in the heart.
MeSH term(s)	Animals ; Mice ; Heart/physiology ; Heart/physiopathology ; Heart Injuries/genetics ; Heart Injuries/metabolism ; Heart Injuries/physiopathology ; Heterogeneous-Nuclear Ribonucleoprotein U/genetics ; Heterogeneous-Nuclear Ribonucleoprotein U/metabolism ; Macrophages/metabolism ; Macrophages/physiology ; Mammals ; Myocardial Infarction/genetics ; Myocardial Infarction/metabolism ; Myocardial Infarction/physiopathology ; Myocytes, Cardiac/metabolism ; Myocytes, Cardiac/physiology ; Neovascularization, Physiologic/genetics ; Neovascularization, Physiologic/physiology ; Regeneration/genetics ; Regeneration/physiology ; RNA, Long Noncoding/genetics ; RNA, Long Noncoding/metabolism
Chemical Substances	Heterogeneous-Nuclear Ribonucleoprotein U ; MALAT1 long non-coding RNA, human ; RNA, Long Noncoding
Language	English
Publishing date	2023-03-08
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	2379-3708
ISSN (online)	2379-3708
DOI	10.1172/jci.insight.162124
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Article ; Online: DNMT3A clonal hematopoiesis-driver mutations induce cardiac fibrosis by paracrine activation of fibroblasts.

Nature communications

2024 Volume 15, Issue 1, Page(s) 606

Abstract: Hematopoietic mutations in epigenetic regulators like DNA methyltransferase 3 alpha (DNMT3A), play a pivotal role in driving clonal hematopoiesis of indeterminate potential (CHIP), and are associated with unfavorable outcomes in patients suffering from ... ...

Abstract	Hematopoietic mutations in epigenetic regulators like DNA methyltransferase 3 alpha (DNMT3A), play a pivotal role in driving clonal hematopoiesis of indeterminate potential (CHIP), and are associated with unfavorable outcomes in patients suffering from heart failure (HF). However, the precise interactions between CHIP-mutated cells and other cardiac cell types remain unknown. Here, we identify fibroblasts as potential partners in interactions with CHIP-mutated monocytes. We used combined transcriptomic data derived from peripheral blood mononuclear cells of HF patients, both with and without CHIP, and cardiac tissue. We demonstrate that inactivation of DNMT3A in macrophages intensifies interactions with cardiac fibroblasts and increases cardiac fibrosis. DNMT3A inactivation amplifies the release of heparin-binding epidermal growth factor-like growth factor, thereby facilitating activation of cardiac fibroblasts. These findings identify a potential pathway of DNMT3A CHIP-driver mutations to the initiation and progression of HF and may also provide a compelling basis for the development of innovative anti-fibrotic strategies.
MeSH term(s)	Humans ; Clonal Hematopoiesis ; DNA (Cytosine-5-)-Methyltransferases/genetics ; DNA Methyltransferase 3A/genetics ; Fibroblasts ; Fibrosis/genetics ; Fibrosis/pathology ; Heart Failure/genetics ; Hematopoiesis/genetics ; Leukocytes, Mononuclear ; Mutation ; Heart Diseases/genetics ; Heart Diseases/pathology
Chemical Substances	DNA (Cytosine-5-)-Methyltransferases (EC 2.1.1.37) ; DNA Methyltransferase 3A (EC 2.1.1.37)
Language	English
Publishing date	2024-01-19
Publishing country	England
Document type	Journal Article
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-023-43003-w
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Article ; Online: Age-Dependent RGS5 Loss in Pericytes Induces Cardiac Dysfunction and Fibrosis.

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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Article ; Online: Notch signalling in ventricular chamber development and cardiomyopathy.

D'Amato, Gaetano / Luxán, Guillermo / de la Pompa, José Luis

The FEBS journal

2016 Volume 283, Issue 23, Page(s) 4223–4237

Abstract: The vertebrate heart is the first organ to form and function during embryogenesis. Primitive streak-derived cardiac progenitors located bilaterally move rostral to form the primitive heart tube that subsequently undergoes rightward looping, remodelling ... ...

Abstract	The vertebrate heart is the first organ to form and function during embryogenesis. Primitive streak-derived cardiac progenitors located bilaterally move rostral to form the primitive heart tube that subsequently undergoes rightward looping, remodelling and septation to give rise to the mature four-chambered heart. Tightly regulated tissue interactions orchestrate the patterning, proliferation and differentiation processes that give rise to the adult ventricles. Studies in animal models have demonstrated the crucial function of the Notch signalling pathway in ventricular development and how alterations in human NOTCH signalling may lead to disease in the form of cardiomyopathies, such as left ventricular noncompaction (LVNC). In this review, we discuss how during trabecular formation and ventricular compaction, Dll4-Notch1 signals from chamber endocardium to regulate cardiomyocyte proliferation and differentiation in a noncell autonomous fashion and how, at later stages, myocardial Jag1 and Jag2 activate Notch1 in chamber endocardium to sustain chamber patterning and compaction with simultaneous coronary vessel development mediated by Dll4-Notch1. We suggest that alterations in these molecular mechanisms underlie MIB1-related familial LVNC and favour the hypothesis that this cardiomyopathy has a congenital nature.
MeSH term(s)	Animals ; Cardiomyopathies/embryology ; Cardiomyopathies/metabolism ; Endocardium/embryology ; Endocardium/metabolism ; Heart Ventricles/embryology ; Heart Ventricles/metabolism ; Humans ; Models, Cardiovascular ; Myocardium/metabolism ; Organogenesis ; Receptors, Notch/metabolism ; Signal Transduction
Chemical Substances	Receptors, Notch
Language	English
Publishing date	2016-12
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2173655-8
ISSN	1742-4658 ; 1742-464X
ISSN (online)	1742-4658
ISSN	1742-464X
DOI	10.1111/febs.13773
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Article ; Online: Post-myocardial infarction heart failure dysregulates the bone vascular niche.

Hoffmann, Jedrzej / Luxán, Guillermo / Abplanalp, Wesley Tyler / Glaser, Simone-Franziska / Rasper, Tina / Fischer, Ariane / Muhly-Reinholz, Marion / Potente, Michael / Assmus, Birgit / John, David / Zeiher, Andreas Michael / Dimmeler, Stefanie

Nature communications

2021 Volume 12, Issue 1, Page(s) 3964

Abstract: The regulation of bone vasculature by chronic diseases, such as heart failure is unknown. Here, we describe the effects of myocardial infarction and post-infarction heart failure on the bone vascular cell composition. We demonstrate an age-independent ... ...

Abstract	The regulation of bone vasculature by chronic diseases, such as heart failure is unknown. Here, we describe the effects of myocardial infarction and post-infarction heart failure on the bone vascular cell composition. We demonstrate an age-independent loss of type H endothelium in heart failure after myocardial infarction in both mice and humans. Using single-cell RNA sequencing, we delineate the transcriptional heterogeneity of human bone marrow endothelium, showing increased expression of inflammatory genes, including IL1B and MYC, in ischemic heart failure. Endothelial-specific overexpression of MYC was sufficient to induce type H bone endothelial cells, whereas inhibition of NLRP3-dependent IL-1β production partially prevented the post-myocardial infarction loss of type H vasculature in mice. These results provide a rationale for using anti-inflammatory therapies to prevent or reverse the deterioration of bone vascular function in ischemic heart disease.
MeSH term(s)	Aged ; Animals ; Bone and Bones/blood supply ; Bone and Bones/physiopathology ; Case-Control Studies ; Endothelial Cells/metabolism ; Endothelial Cells/pathology ; Female ; Furans/pharmacology ; Genes, myc ; Heart Failure/etiology ; Heart Failure/physiopathology ; Hematopoietic Stem Cells/pathology ; Humans ; Indenes/pharmacology ; Inflammation/drug therapy ; Inflammation/metabolism ; Inflammation/pathology ; Interleukin-1beta/genetics ; Interleukin-1beta/metabolism ; Male ; Mice, Inbred C57BL ; Mice, Transgenic ; Middle Aged ; Myocardial Infarction/complications ; Myocardial Infarction/genetics ; Myocardial Infarction/physiopathology ; Platelet Endothelial Cell Adhesion Molecule-1/metabolism ; Sulfonamides/pharmacology ; Mice
Chemical Substances	Furans ; IL1B protein, human ; Indenes ; Interleukin-1beta ; PECAM1 protein, human ; Platelet Endothelial Cell Adhesion Molecule-1 ; Sulfonamides ; N-(1,2,3,5,6,7-hexahydro-S-indacen-4-ylcarbamoyl)-4-(2-hydroxy-2-propanyl)-2-furansulfonamide (6RS86E2BWQ)
Language	English
Publishing date	2021-06-25
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-021-24045-4
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Article ; Online: The splicing-regulatory lncRNA NTRAS sustains vascular integrity.

Fouani, Youssef / Kirchhof, Luisa / Stanicek, Laura / Luxán, Guillermo / Heumüller, Andreas W / Knau, Andrea / Fischer, Ariane / Devraj, Kavi / John, David / Neumann, Philipp / Bindereif, Albrecht / Boon, Reinier A / Liebner, Stefan / Wittig, Ilka / Mogler, Carolin / Karimova, Madina / Dimmeler, Stefanie / Jaé, Nicolas

EMBO reports

2022 Volume 23, Issue 6, Page(s) e54157

Abstract: Vascular integrity is essential for organ homeostasis to prevent edema formation and infiltration of inflammatory cells. Long non-coding RNAs (lncRNAs) are important regulators of gene expression and often expressed in a cell type-specific manner. By ... ...

Abstract	Vascular integrity is essential for organ homeostasis to prevent edema formation and infiltration of inflammatory cells. Long non-coding RNAs (lncRNAs) are important regulators of gene expression and often expressed in a cell type-specific manner. By screening for endothelial-enriched lncRNAs, we identified the undescribed lncRNA NTRAS to control endothelial cell functions. Silencing of NTRAS induces endothelial cell dysfunction in vitro and increases vascular permeability and lethality in mice. Biochemical analysis revealed that NTRAS, through its CA-dinucleotide repeat motif, sequesters the splicing regulator hnRNPL to control alternative splicing of tight junction protein 1 (TJP1; also named zona occludens 1, ZO-1) pre-mRNA. Deletion of the hnRNPL binding motif in mice (Ntras
MeSH term(s)	Alternative Splicing ; Animals ; Endothelial Cells/metabolism ; Mice ; Permeability ; Protein Isoforms/genetics ; RNA, Long Noncoding/genetics ; RNA, Long Noncoding/metabolism ; Tight Junctions/metabolism
Chemical Substances	Protein Isoforms ; RNA, Long Noncoding
Language	English
Publishing date	2022-05-08
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2020896-0
ISSN	1469-3178 ; 1469-221X
ISSN (online)	1469-3178
ISSN	1469-221X
DOI	10.15252/embr.202154157
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Article ; Online: Genetic and functional genomics approaches targeting the Notch pathway in cardiac development and congenital heart disease.

MacGrogan, Donal / Luxán, Guillermo / de la Pompa, José Luis

Briefings in functional genomics

2014 Volume 13, Issue 1, Page(s) 15–27

Abstract: The Notch signalling pathway plays crucial roles in cardiac development and postnatal cardiac homoeostasis. Gain- and loss-of-function approaches indicate that Notch promotes or inhibits cardiogenesis in a stage-dependent manner. However, the molecular ... ...

Abstract	The Notch signalling pathway plays crucial roles in cardiac development and postnatal cardiac homoeostasis. Gain- and loss-of-function approaches indicate that Notch promotes or inhibits cardiogenesis in a stage-dependent manner. However, the molecular mechanisms are poorly defined because many downstream effectors remain to be identified. Genome-scale analyses are shedding light on the genes that are regulated by Notch signalling and the mechanisms underlying this regulation. We review the functional data that implicates Notch in cardiac morphogenetic processes and expression profiling studies that enlighten the regulatory networks behind them. A recurring theme is that Notch cross-talks reiteratively with other key signalling pathways including Wnt and Bmp to coordinate cell and tissue interactions during cardiogenesis.
MeSH term(s)	Animals ; Body Patterning/genetics ; Genomics/methods ; Heart/growth & development ; Heart Defects, Congenital/genetics ; Humans ; Receptors, Notch/metabolism ; Signal Transduction/genetics
Chemical Substances	Receptors, Notch
Language	English
Publishing date	2014-01
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2540916-5
ISSN	2041-2657 ; 2041-2649 ; 2041-2647
ISSN (online)	2041-2657
ISSN	2041-2649 ; 2041-2647
DOI	10.1093/bfgp/elt036
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