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  1. AU="Gowran, Aoife"
  2. AU="Roberta Pastorino"
  3. AU="Ermakov, Alexander S"
  4. AU="YeYun Xin" AU="YeYun Xin"
  5. AU="Giugliani, Camila"
  6. AU=Cerrone Marina
  7. AU="Kohsar, Matin"
  8. AU="Ella Brandt"
  9. AU="Jiwei Wang"
  10. AU="Croda, Júlio Henrique Rosa"
  11. AU="Arkun, Ani"
  12. AU="Fan-tao KONG"
  13. AU="Field, R C"
  14. AU="Coombes, Brandon J"
  15. AU="Garay, Raúl O."
  16. AU="Jingfeng Xue"
  17. AU="Kelliher, Christina M"
  18. AU="Busby, Marjorie G"

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  1. Artikel: The Endocannabinoid System and Cannabidiol: Past, Present, and Prospective for Cardiovascular Diseases.

    Rabino, Martina / Mallia, Sara / Castiglioni, Elisa / Rovina, Davide / Pompilio, Giulio / Gowran, Aoife

    Pharmaceuticals (Basel, Switzerland)

    2021  Band 14, Heft 9

    Abstract: In the past, cannabis was commonly associated with mysticism and illegality. Fortunately, in recent years perspectives and discourses have changed. More prominence has been given to the rigorous scientific effort that led to the discovery of cannabis' ... ...

    Abstract In the past, cannabis was commonly associated with mysticism and illegality. Fortunately, in recent years perspectives and discourses have changed. More prominence has been given to the rigorous scientific effort that led to the discovery of cannabis' many physiological actions and endogenous signalling mechanisms. The endocannabinoid system is a complex and heterogeneous pro-homeostatic network comprising different receptors with several endogenous ligands, numerous metabolic enzymes and regulatory proteins. Therefore, it is not surprising that alterations and dysfunctions of the endocannabinoid system are observed in almost every category of disease. Such high degree of pathophysiological involvement suggests the endocannabinoid system is a promising therapeutic target and prompted the translation of resurgent scientific findings into clinical therapies. Shifting attitudes toward cannabis also raised other matters such as increased patient awareness, prescription requests, self-medication, recreational use, recognition of new knowledge gaps, renewed scientific activity, and seemingly exponential growth of the cannabis industry. This review, following a general overview of cannabis and the endocannabinoid system, assiduously describes its role within the context of cardiovascular diseases, paying particular attention to the Janus influence that endocannabinoid system modulators can have on the cardiovascular system.
    Sprache Englisch
    Erscheinungsdatum 2021-09-17
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article ; Review
    ZDB-ID 2193542-7
    ISSN 1424-8247
    ISSN 1424-8247
    DOI 10.3390/ph14090936
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel: Unchain My Heart: Integrins at the Basis of iPSC Cardiomyocyte Differentiation.

    Santoro, Rosaria / Perrucci, Gianluca Lorenzo / Gowran, Aoife / Pompilio, Giulio

    Stem cells international

    2019  Band 2019, Seite(n) 8203950

    Abstract: The cellular response to the extracellular matrix (ECM) microenvironment mediated by integrin adhesion is of fundamental importance, in both developmental and pathological processes. In particular, mechanotransduction is of growing importance in ... ...

    Abstract The cellular response to the extracellular matrix (ECM) microenvironment mediated by integrin adhesion is of fundamental importance, in both developmental and pathological processes. In particular, mechanotransduction is of growing importance in groundbreaking cellular models such as induced pluripotent stem cells (iPSC), since this process may strongly influence cell fate and, thus, augment the precision of differentiation into specific cell types, e.g., cardiomyocytes. The decryption of the cellular machinery starting from ECM sensing to iPSC differentiation calls for new
    Sprache Englisch
    Erscheinungsdatum 2019-02-13
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Review
    ZDB-ID 2573856-2
    ISSN 1687-9678 ; 1687-966X
    ISSN (online) 1687-9678
    ISSN 1687-966X
    DOI 10.1155/2019/8203950
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  3. Artikel ; Online: "Betwixt Mine Eye and Heart a League Is Took": The Progress of Induced Pluripotent Stem-Cell-Based Models of Dystrophin-Associated Cardiomyopathy.

    Rovina, Davide / Castiglioni, Elisa / Niro, Francesco / Mallia, Sara / Pompilio, Giulio / Gowran, Aoife

    International journal of molecular sciences

    2020  Band 21, Heft 19

    Abstract: The ultimate goal of precision disease modeling is to artificially recreate the disease of affected people in a highly controllable and adaptable external environment. This field has rapidly advanced which is evident from the application of patient- ... ...

    Abstract The ultimate goal of precision disease modeling is to artificially recreate the disease of affected people in a highly controllable and adaptable external environment. This field has rapidly advanced which is evident from the application of patient-specific pluripotent stem-cell-derived precision therapies in numerous clinical trials aimed at a diverse set of diseases such as macular degeneration, heart disease, spinal cord injury, graft-versus-host disease, and muscular dystrophy. Despite the existence of semi-adequate treatments for tempering skeletal muscle degeneration in dystrophic patients, nonischemic cardiomyopathy remains one of the primary causes of death. Therefore, cardiovascular cells derived from muscular dystrophy patients' induced pluripotent stem cells are well suited to mimic dystrophin-associated cardiomyopathy and hold great promise for the development of future fully effective therapies. The purpose of this article is to convey the realities of employing precision disease models of dystrophin-associated cardiomyopathy. This is achieved by discussing, as suggested in the title echoing William Shakespeare's words, the settlements (or "leagues") made by researchers to manage the constraints ("betwixt mine eye and heart") distancing them from achieving a perfect precision disease model.
    Mesh-Begriff(e) Animals ; Cardiomyopathy, Dilated/genetics ; Cardiomyopathy, Dilated/metabolism ; Cardiomyopathy, Dilated/pathology ; Cardiomyopathy, Dilated/therapy ; Clinical Trials as Topic ; Disease Models, Animal ; Dystrophin/genetics ; Dystrophin/metabolism ; Humans ; Induced Pluripotent Stem Cells/metabolism ; Induced Pluripotent Stem Cells/pathology ; Induced Pluripotent Stem Cells/transplantation ; Muscular Dystrophies/genetics ; Muscular Dystrophies/metabolism ; Muscular Dystrophies/therapy ; Myocytes, Cardiac/metabolism ; Myocytes, Cardiac/pathology ; Stem Cell Transplantation
    Chemische Substanzen Dystrophin
    Sprache Englisch
    Erscheinungsdatum 2020-09-23
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article ; Review
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms21196997
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  4. Artikel ; Online: IPSC derived cardiac fibroblasts of DMD patients show compromised actin microfilaments, metabolic shift and pro-fibrotic phenotype.

    Soussi, Salwa / Savchenko, Lesia / Rovina, Davide / Iacovoni, Jason S / Gottinger, Andrea / Vialettes, Maxime / Pioner, Josè-Manuel / Farini, Andrea / Mallia, Sara / Rabino, Martina / Pompilio, Giulio / Parini, Angelo / Lairez, Olivier / Gowran, Aoife / Pizzinat, Nathalie

    Biology direct

    2023  Band 18, Heft 1, Seite(n) 41

    Abstract: Duchenne muscular dystrophy (DMD) is a severe form of muscular dystrophy caused by mutations in the dystrophin gene. We characterized which isoforms of dystrophin were expressed by human induced pluripotent stem cell (hiPSC)-derived cardiac fibroblasts ... ...

    Abstract Duchenne muscular dystrophy (DMD) is a severe form of muscular dystrophy caused by mutations in the dystrophin gene. We characterized which isoforms of dystrophin were expressed by human induced pluripotent stem cell (hiPSC)-derived cardiac fibroblasts obtained from control and DMD patients. Distinct dystrophin isoforms were observed; however, highest molecular weight isoform was absent in DMD patients carrying exon deletions or mutations in the dystrophin gene. The loss of the full-length dystrophin isoform in hiPSC-derived cardiac fibroblasts from DMD patients resulted in deficient formation of actin microfilaments and a metabolic switch from mitochondrial oxidation to glycolysis. The DMD hiPSC-derived cardiac fibroblasts exhibited a dysregulated mitochondria network and reduced mitochondrial respiration, with enhanced compensatory glycolysis to sustain cellular ATP production. This metabolic remodeling was associated with an exacerbated myofibroblast phenotype and increased fibroblast activation in response to pro fibrotic challenges. As cardiac fibrosis is a critical pathological feature of the DMD heart, the myofibroblast phenotype induced by the absence of dystrophin may contribute to deterioration in cardiac function. Our study highlights the relationship between cytoskeletal dynamics, metabolism of the cell and myofibroblast differentiation and provides a new mechanism by which inactivation of dystrophin in non-cardiomyocyte cells may increase the severity of cardiopathy.
    Mesh-Begriff(e) Humans ; Dystrophin/genetics ; Dystrophin/metabolism ; Myocytes, Cardiac/metabolism ; Induced Pluripotent Stem Cells/metabolism ; Induced Pluripotent Stem Cells/pathology ; Muscular Dystrophy, Duchenne/genetics ; Muscular Dystrophy, Duchenne/metabolism ; Muscular Dystrophy, Duchenne/pathology ; Phenotype ; Actin Cytoskeleton/metabolism ; Actin Cytoskeleton/pathology ; Fibroblasts/metabolism ; Fibrosis ; Protein Isoforms/genetics ; Protein Isoforms/metabolism
    Chemische Substanzen Dystrophin ; Protein Isoforms
    Sprache Englisch
    Erscheinungsdatum 2023-07-27
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2221028-3
    ISSN 1745-6150 ; 1745-6150
    ISSN (online) 1745-6150
    ISSN 1745-6150
    DOI 10.1186/s13062-023-00398-2
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  5. Artikel ; Online: Correction: IPSC derived cardiac fibroblasts of DMD patients show compromised actin microfilaments, metabolic shift and pro-fibrotic phenotype.

    Soussi, Salwa / Savchenko, Lesia / Rovina, Davide / Iacovoni, Jason S / Gottinger, Andrea / Vialettes, Maxime / Pioner, Josè-Manuel / Farini, Andrea / Mallia, Sara / Rabino, Martina / Pompilio, Giulio / Parini, Angelo / Lairez, Olivier / Gowran, Aoife / Pizzinat, Nathalie

    Biology direct

    2023  Band 18, Heft 1, Seite(n) 62

    Sprache Englisch
    Erscheinungsdatum 2023-10-07
    Erscheinungsland England
    Dokumenttyp Published Erratum
    ZDB-ID 2221028-3
    ISSN 1745-6150 ; 1745-6150
    ISSN (online) 1745-6150
    ISSN 1745-6150
    DOI 10.1186/s13062-023-00417-2
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  6. Artikel ; Online: Multiomic Approaches to Uncover the Complexities of Dystrophin-Associated Cardiomyopathy.

    Gowran, Aoife / Brioschi, Maura / Rovina, Davide / Chiesa, Mattia / Piacentini, Luca / Mallia, Sara / Banfi, Cristina / Pompilio, Giulio / Santoro, Rosaria

    International journal of molecular sciences

    2021  Band 22, Heft 16

    Abstract: Despite major progress in treating skeletal muscle disease associated with dystrophinopathies, cardiomyopathy is emerging as a major cause of death in people carrying dystrophin gene mutations that remain without a targeted cure even with new treatment ... ...

    Abstract Despite major progress in treating skeletal muscle disease associated with dystrophinopathies, cardiomyopathy is emerging as a major cause of death in people carrying dystrophin gene mutations that remain without a targeted cure even with new treatment directions and advances in modelling abilities. The reasons for the stunted progress in ameliorating dystrophin-associated cardiomyopathy (DAC) can be explained by the difficulties in detecting pathophysiological mechanisms which can also be efficiently targeted within the heart in the widest patient population. New perspectives are clearly required to effectively address the unanswered questions concerning the identification of authentic and effectual readouts of DAC occurrence and severity. A potential way forward to achieve further therapy breakthroughs lies in combining multiomic analysis with advanced preclinical precision models. This review presents the fundamental discoveries made using relevant models of DAC and how omics approaches have been incorporated to date.
    Mesh-Begriff(e) Animals ; Cardiomyopathies/etiology ; Cardiomyopathies/metabolism ; Cardiomyopathies/pathology ; Computational Biology/methods ; Dystrophin/deficiency ; Genome ; Humans ; Proteome/analysis ; Transcriptome
    Chemische Substanzen Dystrophin ; Proteome
    Sprache Englisch
    Erscheinungsdatum 2021-08-19
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article ; Review
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms22168954
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  7. Artikel ; Online: Reprogramming of dermal fibroblasts from a Duchenne muscular dystrophy patient carrying a deletion of exons 45-50 into an induced pluripotent stem cell line (CCMi005-A).

    Rovina, Davide / Castiglioni, Elisa / Mallia, Sara / Rabino, Martina / Farini, Andrea / Belicchi, Marzia / Di Giuseppe, Giusy / Gervasini, Cristina / Torrente, Yvan / Pompilio, Giulio / Gowran, Aoife

    Stem cell research

    2022  Band 64, Seite(n) 102889

    Abstract: Duchenne muscular dystrophy (DMD) is an X-linked syndrome that affects skeletal and cardiac muscle and is caused by mutation of the dystrophin gene. Induced pluripotent stem cells (iPSCs) were generated from dermal fibroblasts by electroporation with ... ...

    Abstract Duchenne muscular dystrophy (DMD) is an X-linked syndrome that affects skeletal and cardiac muscle and is caused by mutation of the dystrophin gene. Induced pluripotent stem cells (iPSCs) were generated from dermal fibroblasts by electroporation with episomal vectors containing the reprogramming factors (OCT4, SOX2, LIN28, KLF4, and l-MYC). The donor carried an out-of-frame deletion of exons 45-50 of the dystrophin gene. The established iPSC line exhibited normal morphology, expressed pluripotency markers, had normal karyotype and possessed trilineage differentiation potential.
    Mesh-Begriff(e) Humans ; Dystrophin/genetics ; Muscular Dystrophy, Duchenne/genetics ; Muscular Dystrophy, Duchenne/metabolism ; Induced Pluripotent Stem Cells/metabolism ; Inducible T-Cell Co-Stimulator Protein/genetics ; Inducible T-Cell Co-Stimulator Protein/metabolism ; Exons/genetics ; Cell Differentiation ; Fibroblasts/metabolism ; Cellular Reprogramming
    Chemische Substanzen Dystrophin ; Inducible T-Cell Co-Stimulator Protein
    Sprache Englisch
    Erscheinungsdatum 2022-08-05
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2393143-7
    ISSN 1876-7753 ; 1873-5061
    ISSN (online) 1876-7753
    ISSN 1873-5061
    DOI 10.1016/j.scr.2022.102889
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  8. Artikel ; Online: The harder the climb the better the view: The impact of substrate stiffness on cardiomyocyte fate.

    Querceto, Silvia / Santoro, Rosaria / Gowran, Aoife / Grandinetti, Bruno / Pompilio, Giulio / Regnier, Michael / Tesi, Chiara / Poggesi, Corrado / Ferrantini, Cecilia / Pioner, Josè Manuel

    Journal of molecular and cellular cardiology

    2022  Band 166, Seite(n) 36–49

    Abstract: The quest for novel methods to mature human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) for cardiac regeneration, modelling and drug testing has emphasized a need to create microenvironments with physiological features. Many studies ... ...

    Abstract The quest for novel methods to mature human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) for cardiac regeneration, modelling and drug testing has emphasized a need to create microenvironments with physiological features. Many studies have reported on how cardiomyocytes sense substrate stiffness and adapt their morphological and functional properties. However, these observations have raised new biological questions and a shared vision to translate it into a tissue or organ context is still elusive. In this review, we will focus on the relevance of substrates mimicking cardiac extracellular matrix (cECM) rigidity for the understanding of the biomechanical crosstalk between the extracellular and intracellular environment. The ability to opportunely modulate these pathways could be a key to regulate in vitro hiPSC-CM maturation. Therefore, both hiPSC-CM models and substrate stiffness appear as intriguing tools for the investigation of cECM-cell interactions. More understanding of these mechanisms may provide novel insights on how cECM affects cardiac cell function in the context of genetic cardiomyopathies.
    Mesh-Begriff(e) Cell Communication ; Cell Differentiation ; Extracellular Matrix/metabolism ; Humans ; Induced Pluripotent Stem Cells/metabolism ; Myocytes, Cardiac/metabolism
    Sprache Englisch
    Erscheinungsdatum 2022-02-06
    Erscheinungsland England
    Dokumenttyp Journal Article ; Review ; 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.2022.02.001
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  9. Artikel: The cannabinoid receptor type 1 is essential for mesenchymal stem cell survival and differentiation: implications for bone health.

    Gowran, Aoife / McKayed, Katey / Campbell, Veronica A

    Stem cells international

    2013  Band 2013, Seite(n) 796715

    Abstract: Significant loss of bone due to trauma, underlying metabolic disease, or lack of repair due to old age surpasses the body's endogenous bone repair mechanisms. Mesenchymal stem cells (MSCs) are adult stem cells which may represent an ideal cell type for ... ...

    Abstract Significant loss of bone due to trauma, underlying metabolic disease, or lack of repair due to old age surpasses the body's endogenous bone repair mechanisms. Mesenchymal stem cells (MSCs) are adult stem cells which may represent an ideal cell type for use in cell-based tissue engineered bone regeneration strategies. The body's endocannabinoid system has been identified as a central regulator of bone metabolism. The aim of the study was to elucidate the role of the cannabinoid receptor type 1 in the differentiation and survival of MSCs. We show that the cannabinoid receptor type 1 has a prosurvival function during acute cell stress. Additionally, we show that the phytocannabinoid, Δ(9)-Tetrahydrocannabinol, has a negative impact on MSC survival and osteogenesis. Overall, these results show the potential for the modulation of the cannabinoid system in cell-based tissue engineered bone regeneration strategies whilst highlighting cannabis use as a potential cause for concern in the management of orthopaedic patients.
    Sprache Englisch
    Erscheinungsdatum 2013-06-24
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ZDB-ID 2573856-2
    ISSN 1687-9678 ; 1687-966X
    ISSN (online) 1687-9678
    ISSN 1687-966X
    DOI 10.1155/2013/796715
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  10. Artikel: Corrigendum: Calcium handling maturation and adaptation to increased substrate stiffness in human iPSC-derived cardiomyocytes: the impact of full-length dystrophin deficiency.

    Pioner, Josè Manuel / Santini, Lorenzo / Palandri, Chiara / Langione, Marianna / Grandinetti, Bruno / Querceto, Silvia / Martella, Daniele / Mazzantini, Costanza / Scellini, Beatrice / Giammarino, Lucrezia / Lupi, Flavia / Mazzarotto, Francesco / Gowran, Aoife / Rovina, Davide / Santoro, Rosaria / Pompilio, Giulio / Tesi, Chiara / Parmeggiani, Camilla / Regnier, Michael /
    Cerbai, Elisabetta / Mack, David L / Poggesi, Corrado / Ferrantini, Cecilia / Coppini, Raffaele

    Frontiers in physiology

    2023  Band 14, Seite(n) 1222400

    Abstract: This corrects the article DOI: 10.3389/fphys.2022.1030920.]. ...

    Abstract [This corrects the article DOI: 10.3389/fphys.2022.1030920.].
    Sprache Englisch
    Erscheinungsdatum 2023-06-13
    Erscheinungsland Switzerland
    Dokumenttyp Published Erratum
    ZDB-ID 2564217-0
    ISSN 1664-042X
    ISSN 1664-042X
    DOI 10.3389/fphys.2023.1222400
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