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  1. Book ; Online ; Thesis: Role of Extracellular ATP in the Progression of Muscle Damage in Sarcoglycanopathies

    Gazzerro, Elisabetta [Verfasser]

    2021  

    Author's details Elisabetta Gazzerro
    Keywords Medizin, Gesundheit ; Medicine, Health
    Subject code sg610
    Language English
    Publisher Medizinische Fakultät Charité - Universitätsmedizin Berlin
    Publishing place Berlin
    Document type Book ; Online ; Thesis
    Database Digital theses on the web

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  2. Article ; Online: Caveolin-3 and Caveolin-1 Interaction Decreases Channel Dysfunction Due to Caveolin-3 Mutations.

    Benzoni, Patrizia / Gazzerro, Elisabetta / Fiorillo, Chiara / Baratto, Serena / Bartolucci, Chiara / Severi, Stefano / Milanesi, Raffaella / Lippi, Melania / Langione, Marianna / Murano, Carmen / Meoni, Clarissa / Popolizio, Vera / Cospito, Alessandro / Baruscotti, Mirko / Bucchi, Annalisa / Barbuti, Andrea

    International journal of molecular sciences

    2024  Volume 25, Issue 2

    Abstract: Caveolae constitute membrane microdomains where receptors and ion channels functionally interact. Caveolin-3 (cav-3) is the key structural component of muscular caveolae. Mutations ... ...

    Abstract Caveolae constitute membrane microdomains where receptors and ion channels functionally interact. Caveolin-3 (cav-3) is the key structural component of muscular caveolae. Mutations in
    MeSH term(s) Adult ; Animals ; Cricetinae ; Humans ; Caveolin 1/genetics ; Caveolin 3/genetics ; Cricetulus ; Mutation ; CHO Cells ; Ion Channels
    Chemical Substances Caveolin 1 ; Caveolin 3 ; Ion Channels
    Language English
    Publishing date 2024-01-12
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms25020980
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Gap Junctions and Epileptogenesis: No Laughing Matter.

    Gazzerro, Elisabetta / Striano, Pasquale

    EBioMedicine

    2016  Volume 8, Page(s) 5–6

    Language English
    Publishing date 2016-05-24
    Publishing country Netherlands
    Document type Journal Article ; Comment
    ZDB-ID 2851331-9
    ISSN 2352-3964
    ISSN (online) 2352-3964
    DOI 10.1016/j.ebiom.2016.05.024
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Aberrant Adenosine Triphosphate Release and Impairment of P2Y2-Mediated Signaling in Sarcoglycanopathies.

    Benzi, Andrea / Baratto, Serena / Astigiano, Cecilia / Sturla, Laura / Panicucci, Chiara / Mamchaoui, Kamel / Raffaghello, Lizzia / Bruzzone, Santina / Gazzerro, Elisabetta / Bruno, Claudio

    Laboratory investigation; a journal of technical methods and pathology

    2023  Volume 103, Issue 3, Page(s) 100037

    Abstract: Sarcoglycanopathies, limb-girdle muscular dystrophies (LGMD) caused by genetic loss-of-function of the membrane proteins sarcoglycans (SGs), are characterized by progressive degeneration of skeletal muscle. In these disorders, muscle necrosis is ... ...

    Abstract Sarcoglycanopathies, limb-girdle muscular dystrophies (LGMD) caused by genetic loss-of-function of the membrane proteins sarcoglycans (SGs), are characterized by progressive degeneration of skeletal muscle. In these disorders, muscle necrosis is associated with immune-mediated damage, whose triggering and perpetuating molecular mechanisms are not fully elucidated yet. Extracellular adenosine triphosphate (eATP) seems to represent a crucial factor, with eATP activating purinergic receptors. Indeed, in vivo blockade of the eATP/P2X7 purinergic pathway ameliorated muscle disease progression. P2X7 inhibition improved the dystrophic process by restraining the activity of P2X7 receptors on immune cells. Whether P2X7 blockade can display a direct action on muscle cells is not known yet. In this study, we investigated eATP effects in primary cultures of myoblasts isolated from patients with LGMDR3 (α-sarcoglycanopathy) and in immortalized cells isolated from a patient with LGMDR5 (γ-sarcoglycanopathy). Our results demonstrated that, owing to a reduced ecto-ATPase activity and/or an enhanced release of ATP, patient cells are exposed to increased juxtamembrane concentrations of eATP and display a higher susceptivity to eATP signals. The purinoceptor P2Y2, which proved to be overexpressed in patient cells, was identified as a pivotal receptor responsible for the enhanced ATP-induced or UTP-induced Ca
    MeSH term(s) Humans ; Adenosine Triphosphate/metabolism ; Muscle, Skeletal/metabolism ; Sarcoglycanopathies/metabolism ; Signal Transduction ; Receptors, Purinergic P2Y2
    Chemical Substances Adenosine Triphosphate (8L70Q75FXE) ; Receptors, Purinergic P2Y2
    Language English
    Publishing date 2023-01-10
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 80178-1
    ISSN 1530-0307 ; 0023-6837
    ISSN (online) 1530-0307
    ISSN 0023-6837
    DOI 10.1016/j.labinv.2022.100037
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article: "suMus," a novel digital system for arm movement metrics and muscle energy expenditure.

    Gerhalter, Teresa / Müller, Christina / Maron, Elke / Thielen, Markus / Schätzl, Teresa / Mähler, Anja / Schütte, Till / Boschmann, Michael / Herzer, René / Spuler, Simone / Gazzerro, Elisabetta

    Frontiers in physiology

    2023  Volume 14, Page(s) 1057592

    Abstract: Objective: ...

    Abstract Objective:
    Language English
    Publishing date 2023-01-26
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2564217-0
    ISSN 1664-042X
    ISSN 1664-042X
    DOI 10.3389/fphys.2023.1057592
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Targeting gut dysbiosis against inflammation and impaired autophagy in Duchenne muscular dystrophy.

    Kalkan, Hilal / Pagano, Ester / Paris, Debora / Panza, Elisabetta / Cuozzo, Mariarosaria / Moriello, Claudia / Piscitelli, Fabiana / Abolghasemi, Armita / Gazzerro, Elisabetta / Silvestri, Cristoforo / Capasso, Raffaele / Motta, Andrea / Russo, Roberto / Di Marzo, Vincenzo / Iannotti, Fabio Arturo

    EMBO molecular medicine

    2023  Volume 15, Issue 3, Page(s) e16225

    Abstract: Nothing is known about the potential implication of gut microbiota in skeletal muscle disorders. Here, we provide evidence that fecal microbiota composition along with circulating levels of short-chain fatty acids (SCFAs) and related metabolites are ... ...

    Abstract Nothing is known about the potential implication of gut microbiota in skeletal muscle disorders. Here, we provide evidence that fecal microbiota composition along with circulating levels of short-chain fatty acids (SCFAs) and related metabolites are altered in the mdx mouse model of Duchenne muscular dystrophy (DMD) compared with healthy controls. Supplementation with sodium butyrate (NaB) in mdx mice rescued muscle strength and autophagy, and prevented inflammation associated with excessive endocannabinoid signaling at CB1 receptors to the same extent as deflazacort (DFZ), the standard palliative care for DMD. In LPS-stimulated C2C12 myoblasts, NaB reduces inflammation, promotes autophagy, and prevents dysregulation of microRNAs targeting the endocannabinoid CB1 receptor gene, in a manner depending on the activation of GPR109A and PPARγ receptors. In sum, we propose a novel disease-modifying approach in DMD that may have benefits also in other muscular dystrophies.
    MeSH term(s) Animals ; Mice ; Autophagy ; Dysbiosis ; Endocannabinoids/metabolism ; Inflammation/metabolism ; Mice, Inbred mdx ; Muscle, Skeletal/metabolism ; Muscular Dystrophy, Duchenne/drug therapy ; Muscular Dystrophy, Duchenne/genetics ; Intestines
    Chemical Substances Endocannabinoids
    Language English
    Publishing date 2023-01-03
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2467145-9
    ISSN 1757-4684 ; 1757-4676
    ISSN (online) 1757-4684
    ISSN 1757-4676
    DOI 10.15252/emmm.202216225
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Targeting gut dysbiosis against inflammation and impaired autophagy in Duchenne muscular dystrophy

    Hilal Kalkan / Ester Pagano / Debora Paris / Elisabetta Panza / Mariarosaria Cuozzo / Claudia Moriello / Fabiana Piscitelli / Armita Abolghasemi / Elisabetta Gazzerro / Cristoforo Silvestri / Raffaele Capasso / Andrea Motta / Roberto Russo / Vincenzo Di Marzo / Fabio Arturo Iannotti

    EMBO Molecular Medicine, Vol 15, Iss 3, Pp n/a-n/a (2023)

    2023  

    Abstract: Abstract Nothing is known about the potential implication of gut microbiota in skeletal muscle disorders. Here, we provide evidence that fecal microbiota composition along with circulating levels of short‐chain fatty acids (SCFAs) and related metabolites ...

    Abstract Abstract Nothing is known about the potential implication of gut microbiota in skeletal muscle disorders. Here, we provide evidence that fecal microbiota composition along with circulating levels of short‐chain fatty acids (SCFAs) and related metabolites are altered in the mdx mouse model of Duchenne muscular dystrophy (DMD) compared with healthy controls. Supplementation with sodium butyrate (NaB) in mdx mice rescued muscle strength and autophagy, and prevented inflammation associated with excessive endocannabinoid signaling at CB1 receptors to the same extent as deflazacort (DFZ), the standard palliative care for DMD. In LPS‐stimulated C2C12 myoblasts, NaB reduces inflammation, promotes autophagy, and prevents dysregulation of microRNAs targeting the endocannabinoid CB1 receptor gene, in a manner depending on the activation of GPR109A and PPARγ receptors. In sum, we propose a novel disease‐modifying approach in DMD that may have benefits also in other muscular dystrophies.
    Keywords autophagy ; duchenne muscular dystrophy ; endocannabinoid system ; gut microbiota ; short‐chain fatty acids ; Medicine (General) ; R5-920 ; Genetics ; QH426-470
    Subject code 571
    Language English
    Publishing date 2023-03-01T00:00:00Z
    Publisher Wiley
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  8. Article ; Online: Gap Junctions and Epileptogenesis

    Elisabetta Gazzerro / Pasquale Striano

    EBioMedicine, Vol 8, Iss C, Pp 5-

    No Laughing Matter

    2016  Volume 6

    Keywords Medicine ; R ; Medicine (General) ; R5-920
    Language English
    Publishing date 2016-06-01T00:00:00Z
    Publisher Elsevier
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  9. Article ; Online: Diagnostik und Therapie von statinassoziierten Muskelsymptomen.

    Kassner, Ursula / Grunwald, Stefanie / Spira, Dominik / Buchmann, Nikolaus / Bobbert, Thomas / Gazzerro, Elisabetta / Hollstein, Tim / Spuler, Simone / Steinhagen-Thiessen, Elisabeth

    Der Internist

    2021  Volume 62, Issue 8, Page(s) 827–840

    Abstract: Statins are among the most frequently prescribed drugs in Germany. Their benefits in lowering cardiovascular risk are beyond dispute. Nevertheless, many patients complain of side effects from statin therapy, including statin-associated muscle symptoms ( ... ...

    Title translation Diagnostics and treatment of statin-associated muscle symptoms.
    Abstract Statins are among the most frequently prescribed drugs in Germany. Their benefits in lowering cardiovascular risk are beyond dispute. Nevertheless, many patients complain of side effects from statin therapy, including statin-associated muscle symptoms (SAMS) in particular. Despite their relative frequency, it is difficult to objectively diagnose them, as the time until appearance of first symptoms, the nature of the complaints and the severity of muscle problems vary widely. This narrative review summarizes the causes of SAMS as well as new possibilities regarding their diagnosis and therapy.
    Language German
    Publishing date 2021-06-18
    Publishing country Germany
    Document type English Abstract ; Journal Article
    ZDB-ID 2913-0
    ISSN 1432-1289 ; 0020-9554
    ISSN (online) 1432-1289
    ISSN 0020-9554
    DOI 10.1007/s00108-021-01059-0
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Skeletal actions of insulin-like growth factors.

    Gazzerro, Elisabetta / Canalis, Ernesto

    Expert review of endocrinology & metabolism

    2014  Volume 1, Issue 1, Page(s) 47–56

    Abstract: Insulin-like growth factors (IGFs) promote longitudinal growth and display anabolic effects in adult bone by acting through endocrine and autocrine/paracrine mechanisms. Binding of IGF-I to its specific tyrosine-kinase receptor leads to interaction with ... ...

    Abstract Insulin-like growth factors (IGFs) promote longitudinal growth and display anabolic effects in adult bone by acting through endocrine and autocrine/paracrine mechanisms. Binding of IGF-I to its specific tyrosine-kinase receptor leads to interaction with the intracellular proteins, insulin receptor substrate-1 and -2, and the activation of distinct intracellular signaling pathways. In cartilage, IGF-I regulates the differentiation of chondrocytes and stimulates the synthesis of components of the extracellular matrix. In bone tissue, IGF-I increases the function of the differentiated osteoblasts and mediates selected anabolic actions of parathyroid hormone. Genetically modified mice, in which selected components of the IGF system were targeted in a tissue-specific fashion, have documented that circulating IGF-I is essential for physiological skeletal growth and adult bone remodeling and that local autocrine/paracrine IGF-I activities are required for optimal trabecular bone mass and mineralization. Studies in humans have indicated a correlation between serum IGF-I levels and bone mineral density. However, there is little information on the use of IGF-I in patients with metabolic bone disease.
    Language English
    Publishing date 2014-01-23
    Publishing country England
    Document type Journal Article
    ISSN 1744-8417
    ISSN (online) 1744-8417
    DOI 10.1586/17446651.1.1.47
    Database MEDical Literature Analysis and Retrieval System OnLINE

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