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Article: Cardiomyocytes Cellular Phenotypes After Myocardial Infarction.

Lodrini, Alessandra Maria / Goumans, Marie-José

2021 Volume 8, Page(s) 750510

Abstract: Despite the increasing success of interventional coronary reperfusion strategies, mortality related to acute myocardial infarction (MI) is still substantial. MI is defined as sudden death of myocardial tissue caused by an ischemic episode. Ischaemia ... ...

Abstract	Despite the increasing success of interventional coronary reperfusion strategies, mortality related to acute myocardial infarction (MI) is still substantial. MI is defined as sudden death of myocardial tissue caused by an ischemic episode. Ischaemia leads to adverse remodelling in the affected myocardium, inducing metabolic and ionic perturbations at a single cell level, ultimately leading to cell death. The adult mammalian heart has limited regenerative capacity to replace lost cells. Identifying and enhancing physiological cardioprotective processes may be a promising therapy for patients with MI. Studies report an increasing amount of evidence stating the intricacy of the pathophysiology of the infarcted heart. Besides apoptosis, other cellular phenotypes have emerged as key players in the ischemic myocardium, in particular senescence, inflammation, and dedifferentiation. Furthermore, some cardiomyocytes in the infarct border zone uncouple from the surviving myocardium and dedifferentiate, while other cells become senescent in response to injury and start to produce a pro-inflammatory secretome. Enhancing electric coupling between cardiomyocytes in the border zone, eliminating senescent cells with senolytic compounds, and upregulating cardioprotective cellular processes like autophagy, may increase the number of functional cardiomyocytes and therefore enhance cardiac contractility. This review describes the different cellular phenotypes and pathways implicated in injury, remodelling, and regeneration of the myocardium after MI. Moreover, we discuss implications of the complex pathophysiological attributes of the infarcted heart in designing new therapeutic strategies.
Language	English
Publishing date	2021-11-08
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2781496-8
ISSN	2297-055X
ISSN	2297-055X
DOI	10.3389/fcvm.2021.750510
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Go with the flow…..

Quax, Paul H A / Goumans, Marie-José T H

Vascular biology (Bristol, England)

2022 Volume 4, Issue 1, Page(s) E1–E2

Language	English
Publishing date	2022-08-18
Publishing country	England
Document type	Editorial
ISSN	2516-5658
ISSN (online)	2516-5658
DOI	10.1530/VB-22-0019
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Article ; Online: SMAD6-deficiency in human genetic disorders.

Luyckx, Ilse / Verstraeten, Aline / Goumans, Marie-José / Loeys, Bart

NPJ genomic medicine

2022 Volume 7, Issue 1, Page(s) 68

Abstract: SMAD6 encodes an intracellular inhibitor of the bone morphogenetic protein (BMP) signalling pathway. Until now, SMAD6-deficiency has been associated with three distinctive human congenital conditions, i.e., congenital heart diseases, including left ... ...

Abstract	SMAD6 encodes an intracellular inhibitor of the bone morphogenetic protein (BMP) signalling pathway. Until now, SMAD6-deficiency has been associated with three distinctive human congenital conditions, i.e., congenital heart diseases, including left ventricular obstruction and conotruncal defects, craniosynostosis and radioulnar synostosis. Intriguingly, a similar spectrum of heterozygous loss-of-function variants has been reported to cause these clinically distinct disorders without a genotype-phenotype correlation. Even identical nucleotide changes have been described in patients with either a cardiovascular phenotype, craniosynostosis or radioulnar synostosis. These findings suggest that the primary pathogenic variant alone cannot explain the resultant patient phenotype. In this review, we summarise clinical and (patho)genetic (dis)similarities between these three SMAD6-related conditions, compare published Madh6 mouse models, in which the importance and impact of the genetic background with respect to the observed phenotype is highlighted, and elaborate on the cellular key mechanisms orchestrated by SMAD6 in the development of these three discrete inherited disorders. In addition, we discuss future research needed to elucidate the pathogenetic mechanisms underlying these diseases in order to improve their molecular diagnosis, advance therapeutic strategies and facilitate counselling of patients and their families.
Language	English
Publishing date	2022-11-21
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2813848-X
ISSN	2056-7944 ; 2056-7944
ISSN (online)	2056-7944
ISSN	2056-7944
DOI	10.1038/s41525-022-00338-5
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Article ; Online: Angiogenesis in Chronic Thromboembolic Pulmonary Hypertension: A Janus-Faced Player?

Willems, Lynn / Kurakula, Kondababu / Verhaegen, Janne / Klok, Frederikus A / Delcroix, Marion / Goumans, Marie-José / Quarck, Rozenn

Arteriosclerosis, thrombosis, and vascular biology

2024 Volume 44, Issue 4, Page(s) 794–806

Abstract: Chronic thromboembolic pulmonary hypertension (CTEPH) is a rare form of pulmonary hypertension characterized by the presence of organized thrombi that obstruct pulmonary arteries, ultimately leading to right heart failure and death. Among others, ... ...

Abstract	Chronic thromboembolic pulmonary hypertension (CTEPH) is a rare form of pulmonary hypertension characterized by the presence of organized thrombi that obstruct pulmonary arteries, ultimately leading to right heart failure and death. Among others, impaired angiogenesis and inflammatory thrombosis have been shown to contribute to the progression of CTEPH. In this review, we summarize the 2-faced nature of angiogenesis in both thrombus formation and resolution in the context of CTEPH and highlight the dual role of angiogenesis and neovascularization in resolving venous thrombi. Furthermore, we discuss relevant in vitro and in vivo models that support the benefits or drawbacks of angiogenesis in CTEPH progression. We discuss the key pathways involved in modulating angiogenesis, particularly the underexplored role of TGFβ (transforming growth factor-beta) signaling in driving fibrosis as an integral element of CTEPH pathogenesis. We finally explore innovative treatment strategies that target angiogenic pathways. These strategies have the potential to pioneer preventive, inventive, or alternative therapeutic options for patients with CTEPH who may not qualify for surgical interventions. Moreover, they could be used synergistically with established treatments such as pulmonary endarterectomy or balloon pulmonary angioplasty. In summary, this review emphasizes the crucial role of angiogenesis in the development of in fibrothrombotic tissue, a major pathological characteristic of CTEPH.
MeSH term(s)	Humans ; Hypertension, Pulmonary/etiology ; Pulmonary Embolism/therapy ; Angiogenesis ; Pulmonary Artery/pathology ; Thrombosis/pathology ; Chronic Disease ; Endarterectomy/adverse effects
Language	English
Publishing date	2024-02-08
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1221433-4
ISSN	1524-4636 ; 1079-5642
ISSN (online)	1524-4636
ISSN	1079-5642
DOI	10.1161/ATVBAHA.123.319852
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Article ; Online: Sex-biased TGFβ signalling in pulmonary arterial hypertension.

Wits, Marius / Becher, Clarissa / de Man, Frances / Sanchez-Duffhues, Gonzalo / Goumans, Marie-José

Cardiovascular research

2023 Volume 119, Issue 13, Page(s) 2262–2277

Abstract: Pulmonary arterial hypertension (PAH) is a rare cardiovascular disorder leading to pulmonary hypertension and, often fatal, right heart failure. Sex differences in PAH are evident, which primarily presents with a female predominance and increased male ... ...

Abstract	Pulmonary arterial hypertension (PAH) is a rare cardiovascular disorder leading to pulmonary hypertension and, often fatal, right heart failure. Sex differences in PAH are evident, which primarily presents with a female predominance and increased male severity. Disturbed signalling of the transforming growth factor-β (TGFβ) family and gene mutations in the bone morphogenetic protein receptor 2 (BMPR2) are risk factors for PAH development, but how sex-specific cues affect the TGFβ family signalling in PAH remains poorly understood. In this review, we aim to explore the sex bias in PAH by examining sex differences in the TGFβ signalling family through mechanistical and translational evidence. Sex hormones including oestrogens, progestogens, and androgens, can determine the expression of receptors (including BMPR2), ligands, and soluble antagonists within the TGFβ family in a tissue-specific manner. Furthermore, sex-related genetic processes, i.e. Y-chromosome expression and X-chromosome inactivation, can influence the TGFβ signalling family at multiple levels. Given the clinical and mechanistical similarities, we expect that the conclusions arising from this review may apply also to hereditary haemorrhagic telangiectasia (HHT), a rare vascular disorder affecting the TGFβ signalling family pathway. In summary, we anticipate that investigating the TGFβ signalling family in a sex-specific manner will contribute to further understand the underlying processes leading to PAH and likely HHT.
MeSH term(s)	Female ; Male ; Humans ; Pulmonary Arterial Hypertension ; Transforming Growth Factor beta/metabolism ; Familial Primary Pulmonary Hypertension ; Hypertension, Pulmonary ; Signal Transduction ; Bone Morphogenetic Protein Receptors, Type II/genetics ; Bone Morphogenetic Protein Receptors, Type II/metabolism
Chemical Substances	Transforming Growth Factor beta ; Bone Morphogenetic Protein Receptors, Type II (EC 2.7.11.30)
Language	English
Publishing date	2023-08-16
Publishing country	England
Document type	Review ; 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/cvad129
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Zs.A 565: Show issues

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bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

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Article ; Online: Single-cell analysis of human fetal epicardium reveals its cellular composition and identifies CRIP1 as a modulator of EMT.

Streef, Thomas J / Groeneveld, Esmee J / van Herwaarden, Tessa / Hjortnaes, Jesper / Goumans, Marie José / Smits, Anke M

Stem cell reports

2023 Volume 18, Issue 7, Page(s) 1421–1435

Abstract: The epicardium plays an essential role in cardiogenesis by providing cardiac cell types and paracrine cues to the developing myocardium. The human adult epicardium is quiescent, but recapitulation of developmental features may contribute to adult cardiac ...

Abstract	The epicardium plays an essential role in cardiogenesis by providing cardiac cell types and paracrine cues to the developing myocardium. The human adult epicardium is quiescent, but recapitulation of developmental features may contribute to adult cardiac repair. The cell fate of epicardial cells is proposed to be determined by the developmental persistence of specific subpopulations. Reports on this epicardial heterogeneity have been inconsistent, and data regarding the human developing epicardium are scarce. Here we specifically isolated human fetal epicardium and used single-cell RNA sequencing to define its composition and to identify regulators of developmental processes. Few specific subpopulations were observed, but a clear distinction between epithelial and mesenchymal cells was present, resulting in novel population-specific markers. Additionally, we identified CRIP1 as a previously unknown regulator involved in epicardial epithelial-to-mesenchymal transition. Overall, our human fetal epicardial cell-enriched dataset provides an excellent platform to study the developing epicardium in great detail.
MeSH term(s)	Adult ; Humans ; Pericardium/metabolism ; Myocardium/metabolism ; Epithelial-Mesenchymal Transition ; Fetus/metabolism ; Single-Cell Analysis ; Carrier Proteins/metabolism ; LIM Domain Proteins/metabolism
Chemical Substances	CRIP1 protein, human ; Carrier Proteins ; LIM Domain Proteins
Language	English
Publishing date	2023-06-29
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2720528-9
ISSN	2213-6711 ; 2213-6711
ISSN (online)	2213-6711
ISSN	2213-6711
DOI	10.1016/j.stemcr.2023.06.002
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Article ; Online: Steering cell orientation through light-based spatiotemporal modulation of the mechanical environment.

Jorba, Ignasi / Gussenhoven, Sil / van der Pol, Atze / Groenen, Bart Gw / van Zon, Maarten / Goumans, Marie José / Kurniawan, Nicholas A / Ristori, Tommaso / Bouten, Carlijn Vc

Biofabrication

2024 Volume 16, Issue 3

Abstract: The anisotropic organization of cells and the extracellular matrix (ECM) is essential for the physiological function of numerous biological tissues, including the myocardium. This organization changes gradually in space and time, during disease ... ...

Abstract	The anisotropic organization of cells and the extracellular matrix (ECM) is essential for the physiological function of numerous biological tissues, including the myocardium. This organization changes gradually in space and time, during disease progression such as myocardial infarction. The role of mechanical stimuli has been demonstrated to be essential in obtaining, maintaining and de-railing this organization, but the underlying mechanisms are scarcely known. To enable the study of the mechanobiological mechanisms involved,
MeSH term(s)	Tissue Engineering/methods ; Extracellular Matrix ; Myocardium ; Heart ; Fibroblasts
Language	English
Publishing date	2024-04-16
Publishing country	England
Document type	Journal Article
ZDB-ID	2500944-8
ISSN	1758-5090 ; 1758-5082
ISSN (online)	1758-5090
ISSN	1758-5082
DOI	10.1088/1758-5090/ad3aa6
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Article ; Online: Mechanical stimulation of induced pluripotent stem derived cardiac fibroblasts.

Bekedam, Fjodor T / Smal, Rowan / Smit, Marisa C / Aman, Jurjan / Vonk-Noordegraaf, Anton / Bogaard, Harm Jan / Goumans, Marie José / De Man, Frances S / Llucià-Valldeperas, Aida

Scientific reports

2024 Volume 14, Issue 1, Page(s) 9795

Abstract: Cardiac fibrosis contributes to the development of heart failure, and is the response of cardiac fibroblasts (CFs) to pressure or volume overload. Limiting factors in CFs research are the poor availability of human cells and the tendency of CFs to ... ...

Abstract	Cardiac fibrosis contributes to the development of heart failure, and is the response of cardiac fibroblasts (CFs) to pressure or volume overload. Limiting factors in CFs research are the poor availability of human cells and the tendency of CFs to transdifferentiate into myofibroblasts when cultured in vitro. The possibility to generate CFs from induced pluripotent stem cells (iPSC), providing a nearly unlimited cell source, opens new possibilities. However, the behaviour of iPSC-CFs under mechanical stimulation has not been studied yet. Our study aimed to assess the behaviour of iPSC-CFs under mechanical stretch and pro-fibrotic conditions. First, we confirm that iPSC-CFs are comparable to primary CFs at gene, protein and functional level. Furthermore, iPSC-derived CFs adopt a pro-fibrotic response to transforming growth factor beta (TGF-β). In addition, mechanical stretch inhibits TGF-β-induced fibroblast activation in iPSC-CFs. Thus, the responsiveness to cytokines and mechanical stimulation of iPSC-CFs demonstrates they possess key characteristics of primary CFs and may be useful for disease modelling.
MeSH term(s)	Induced Pluripotent Stem Cells/cytology ; Induced Pluripotent Stem Cells/metabolism ; Humans ; Fibroblasts/metabolism ; Fibroblasts/cytology ; Transforming Growth Factor beta/metabolism ; Transforming Growth Factor beta/pharmacology ; Stress, Mechanical ; Cells, Cultured ; Cell Differentiation ; Myocardium/cytology ; Myocardium/metabolism ; Myofibroblasts/metabolism ; Myofibroblasts/cytology ; Fibrosis
Chemical Substances	Transforming Growth Factor beta
Language	English
Publishing date	2024-04-29
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-024-60102-w
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Article ; Online: Epicardial TGFβ and BMP Signaling in Cardiac Regeneration: What Lesson Can We Learn from the Developing Heart?

Dronkers, Esther / Wauters, Manon M M / Goumans, Marie José / Smits, Anke M

Biomolecules

2020 Volume 10, Issue 3

Abstract: The epicardium, the outer layer of the heart, has been of interest in cardiac research due to its vital role in the developing and diseased heart. During development, epicardial cells are active and supply cells and paracrine cues to the myocardium. In ... ...

Abstract	The epicardium, the outer layer of the heart, has been of interest in cardiac research due to its vital role in the developing and diseased heart. During development, epicardial cells are active and supply cells and paracrine cues to the myocardium. In the injured adult heart, the epicardium is re-activated and recapitulates embryonic behavior that is essential for a proper repair response. Two indispensable processes for epicardial contribution to heart tissue formation are epithelial to mesenchymal transition (EMT), and tissue invasion. One of the key groups of cytokines regulating both EMT and invasion is the transforming growth factor β (TGFβ) family, including TGFβ and Bone Morphogenetic Protein (BMP). Abundant research has been performed to understand the role of TGFβ family signaling in the developing epicardium. However, less is known about signaling in the adult epicardium. This review provides an overview of the current knowledge on the role of TGFβ in epicardial behavior both in the development and in the repair of the heart. We aim to describe the presence of involved ligands and receptors to establish if and when signaling can occur. Finally, we discuss potential targets to improve the epicardial contribution to cardiac repair as a starting point for future investigation.
MeSH term(s)	Animals ; Bone Morphogenetic Proteins/metabolism ; Epithelial-Mesenchymal Transition ; Humans ; Pericardium/physiology ; Regeneration ; Signal Transduction ; Transforming Growth Factor beta/metabolism
Chemical Substances	Bone Morphogenetic Proteins ; Transforming Growth Factor beta
Language	English
Publishing date	2020-03-05
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2701262-1
ISSN	2218-273X ; 2218-273X
ISSN (online)	2218-273X
ISSN	2218-273X
DOI	10.3390/biom10030404
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Article ; Online: Endoglin: Beyond the Endothelium.

Schoonderwoerd, Mark J A / Goumans, Marie-Jose T H / Hawinkels, Lukas J A C

Biomolecules

2020 Volume 10, Issue 2

Abstract: Keywords: ...

Abstract	Keywords:
MeSH term(s)	Activin Receptors, Type II/metabolism ; Adaptive Immunity ; Animals ; Antibodies, Monoclonal/pharmacology ; Clinical Trials as Topic ; Endoglin/metabolism ; Endothelium/metabolism ; Epithelial Cells/metabolism ; Fibrosis ; Growth Differentiation Factor 2/metabolism ; Hematopoiesis ; Humans ; Immunity, Innate ; Ligands ; Mesenchymal Stem Cells/cytology ; Mice ; Neoplasms/metabolism ; Neovascularization, Pathologic ; Phosphorylation ; Signal Transduction ; Transforming Growth Factor beta/metabolism ; Tumor Microenvironment
Chemical Substances	Antibodies, Monoclonal ; ENG protein, human ; Endoglin ; GDF2 protein, human ; Growth Differentiation Factor 2 ; Ligands ; Transforming Growth Factor beta ; ACVRL1 protein, human (EC 2.7.11.30) ; Activin Receptors, Type II (EC 2.7.11.30) ; carotuximab (YB2EWE6139)
Language	English
Publishing date	2020-02-12
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2701262-1
ISSN	2218-273X ; 2218-273X
ISSN (online)	2218-273X
ISSN	2218-273X
DOI	10.3390/biom10020289
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