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  1. Article ; Online: Cardiac Cell Therapy Rejuvenates the Infarcted Rodent Heart via Direct Injection but Not by Vascular Infusion.

    Vagnozzi, Ronald J / Sargent, Michelle A / Molkentin, Jeffery D

    Circulation

    2020  Volume 141, Issue 12, Page(s) 1037–1039

    MeSH term(s) Animals ; Cell- and Tissue-Based Therapy/methods ; Disease Models, Animal ; Injections ; Myocytes, Cardiac/pathology ; Rodentia
    Language English
    Publishing date 2020-03-23
    Publishing country United States
    Document type Letter ; Research Support, N.I.H., Extramural ; 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.119.044686
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Ui IV Zs.60: Show issues Location:
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  2. Article ; Online: Cardiac Cell Therapy Fails to Rejuvenate the Chronically Scarred Rodent Heart.

    Vagnozzi, Ronald J / Kasam, Rajesh K / Sargent, Michelle A / Molkentin, Jeffery D

    Circulation

    2021  Volume 144, Issue 4, Page(s) 328–331

    MeSH term(s) Animals ; Bone Marrow Cells ; Bone Marrow Transplantation ; Cardiomyopathy, Restrictive/diagnosis ; Cardiomyopathy, Restrictive/etiology ; Cardiomyopathy, Restrictive/therapy ; Cell- and Tissue-Based Therapy/methods ; Chronic Disease ; Disease Models, Animal ; Female ; Fibrosis ; Ischemia/complications ; Male ; Mice ; Rodentia ; Stem Cell Transplantation ; Treatment Failure ; Treatment Outcome
    Language English
    Publishing date 2021-07-26
    Publishing country United States
    Document type Letter ; 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.120.053080
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Ui IV Zs.60: Show issues Location:
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  3. Article ; Online: ANT-dependent MPTP underlies necrotic myofiber death in muscular dystrophy.

    Bround, Michael J / Havens, Julian R / York, Allen J / Sargent, Michelle A / Karch, Jason / Molkentin, Jeffery D

    Science advances

    2023  Volume 9, Issue 34, Page(s) eadi2767

    Abstract: Mitochondrial permeability transition pore (MPTP) formation contributes to ischemia-reperfusion injury in the heart and several degenerative diseases, including muscular dystrophy (MD). MD is a family of genetic disorders characterized by progressive ... ...

    Abstract Mitochondrial permeability transition pore (MPTP) formation contributes to ischemia-reperfusion injury in the heart and several degenerative diseases, including muscular dystrophy (MD). MD is a family of genetic disorders characterized by progressive muscle necrosis and premature death. It has been proposed that the MPTP has two molecular components, the adenine nucleotide translocase (ANT) family of proteins and an unknown component that requires the chaperone cyclophilin D (CypD) to activate. This model was examined in vivo by deleting the gene encoding ANT1 (
    MeSH term(s) Animals ; Mice ; Muscular Dystrophies ; Necrosis ; Cell Death ; Peptidyl-Prolyl Isomerase F ; Disease Models, Animal
    Chemical Substances Peptidyl-Prolyl Isomerase F
    Language English
    Publishing date 2023-08-25
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2810933-8
    ISSN 2375-2548 ; 2375-2548
    ISSN (online) 2375-2548
    ISSN 2375-2548
    DOI 10.1126/sciadv.adi2767
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: A human FLII gene variant alters sarcomeric actin thin filament length and predisposes to cardiomyopathy.

    Kuwabara, Yasuhide / York, Allen J / Lin, Suh-Chin / Sargent, Michelle A / Grimes, Kelly M / Pirruccello, James P / Molkentin, Jeffery D

    Proceedings of the National Academy of Sciences of the United States of America

    2023  Volume 120, Issue 19, Page(s) e2213696120

    Abstract: To better understand the genetic basis of heart disease, we identified a variant in ... ...

    Abstract To better understand the genetic basis of heart disease, we identified a variant in the
    MeSH term(s) Humans ; Animals ; Mice ; Actins/metabolism ; Sarcomeres/metabolism ; Genome-Wide Association Study ; Actin Cytoskeleton/metabolism ; Cardiomyopathies/metabolism ; Mammals/genetics ; Microfilament Proteins/metabolism ; Trans-Activators/metabolism ; Tropomodulin/metabolism ; Cytoskeletal Proteins/metabolism ; Muscle Proteins/metabolism
    Chemical Substances Actins ; FLII protein, human ; Microfilament Proteins ; Trans-Activators ; TMOD1 protein, human ; Tropomodulin ; leiomodin protein, mouse ; Cytoskeletal Proteins ; Muscle Proteins ; FlII protein, mouse
    Language English
    Publishing date 2023-05-01
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 209104-5
    ISSN 1091-6490 ; 0027-8424
    ISSN (online) 1091-6490
    ISSN 0027-8424
    DOI 10.1073/pnas.2213696120
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1148: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    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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  5. Article ; Online: Thbs1 regulates skeletal muscle mass in a TGFβ-Smad2/3-ATF4-dependent manner.

    Vanhoutte, Davy / Schips, Tobias G / Minerath, Rachel A / Huo, Jiuzhou / Kavuri, Naga Swathi Sree / Prasad, Vikram / Lin, Suh-Chin / Bround, Michael J / Sargent, Michelle A / Adams, Christopher M / Molkentin, Jeffery D

    Cell reports

    2024  Volume 43, Issue 5, Page(s) 114149

    Abstract: Loss of muscle mass is a feature of chronic illness and aging. Here, we report that skeletal muscle-specific thrombospondin-1 transgenic mice (Thbs1 Tg) have profound muscle atrophy with age-dependent decreases in exercise capacity and premature ... ...

    Abstract Loss of muscle mass is a feature of chronic illness and aging. Here, we report that skeletal muscle-specific thrombospondin-1 transgenic mice (Thbs1 Tg) have profound muscle atrophy with age-dependent decreases in exercise capacity and premature lethality. Mechanistically, Thbs1 activates transforming growth factor β (TGFβ)-Smad2/3 signaling, which also induces activating transcription factor 4 (ATF4) expression that together modulates the autophagy-lysosomal pathway (ALP) and ubiquitin-proteasome system (UPS) to facilitate muscle atrophy. Indeed, myofiber-specific inhibition of TGFβ-receptor signaling represses the induction of ATF4, normalizes ALP and UPS, and partially restores muscle mass in Thbs1 Tg mice. Similarly, myofiber-specific deletion of Smad2 and Smad3 or the Atf4 gene antagonizes Thbs1-induced muscle atrophy. More importantly, Thbs1
    Language English
    Publishing date 2024-04-26
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2649101-1
    ISSN 2211-1247 ; 2211-1247
    ISSN (online) 2211-1247
    ISSN 2211-1247
    DOI 10.1016/j.celrep.2024.114149
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article: Rpl3l

    Grimes, Kelly M / Prasad, Vikram / Huo, Jiuzhou / Kuwabara, Yasuhide / Vanhoutte, Davy / Baldwin, Tanya A / Bowers, Stephanie L K / Johansen, Anne Katrine Z / Sargent, Michelle A / Lin, Suh-Chin J / Molkentin, Jeffery D

    Frontiers in physiology

    2023  Volume 14, Page(s) 1054169

    Abstract: Introduction: ...

    Abstract Introduction:
    Language English
    Publishing date 2023-01-17
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2564217-0
    ISSN 1664-042X
    ISSN 1664-042X
    DOI 10.3389/fphys.2023.1054169
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Col1a2

    Bowers, Stephanie L K / Meng, Qinghang / Kuwabara, Yasuhide / Huo, Jiuzhou / Minerath, Rachel / York, Allen J / Sargent, Michelle A / Prasad, Vikram / Saviola, Anthony J / Galindo, David Ceja / Hansen, Kirk C / Vagnozzi, Ronald J / Yutzey, Katherine E / Molkentin, Jeffery D

    Cells

    2023  Volume 12, Issue 17

    Abstract: Rationale: The adult cardiac extracellular matrix (ECM) is largely comprised of type I collagen. In addition to serving as the primary structural support component of the cardiac ECM, type I collagen also provides an organizational platform for other ... ...

    Abstract Rationale: The adult cardiac extracellular matrix (ECM) is largely comprised of type I collagen. In addition to serving as the primary structural support component of the cardiac ECM, type I collagen also provides an organizational platform for other ECM proteins, matricellular proteins, and signaling components that impact cellular stress sensing in vivo.
    Objective: Here we investigated how the content and integrity of type I collagen affect cardiac structure function and response to injury.
    Methods and results: We generated and characterized
    Conclusions: Defective type I collagen in the heart alters the structural integrity of the ECM and leads to cardiomyopathy in adulthood, with fibroblast expansion, activation, and alternate fibrotic ECM deposition. However, acute inhibition of type I collagen production can have an anti-fibrotic and anti-hypertrophic effect.
    MeSH term(s) Animals ; Mice ; Cardiomegaly/genetics ; Cardiomyopathies ; Collagen Type I/genetics ; Fibrosis
    Chemical Substances Collagen Type I ; Collagen Type I, alpha2 Subunit ; Col1a2 protein, mouse
    Language English
    Publishing date 2023-08-30
    Publishing country Switzerland
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2661518-6
    ISSN 2073-4409 ; 2073-4409
    ISSN (online) 2073-4409
    ISSN 2073-4409
    DOI 10.3390/cells12172174
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: ERK1/2 signaling induces skeletal muscle slow fiber-type switching and reduces muscular dystrophy disease severity.

    Boyer, Justin G / Prasad, Vikram / Song, Taejeong / Lee, Donghoon / Fu, Xing / Grimes, Kelly M / Sargent, Michelle A / Sadayappan, Sakthivel / Molkentin, Jeffery D

    JCI insight

    2019  Volume 5

    Abstract: Mitogen-activated protein kinase (MAPK) signaling consists of an array of successively acting kinases. The extracellular signal-regulated kinases 1/2 (ERK1/2) are major components of the greater MAPK cascade that transduce growth factor signaling at the ... ...

    Abstract Mitogen-activated protein kinase (MAPK) signaling consists of an array of successively acting kinases. The extracellular signal-regulated kinases 1/2 (ERK1/2) are major components of the greater MAPK cascade that transduce growth factor signaling at the cell membrane. Here we investigated ERK1/2 signaling in skeletal muscle homeostasis and disease. Using mouse genetics, we observed that the muscle-specific expression of a constitutively active MEK1 mutant promotes greater ERK1/2 signaling that mediates fiber-type switching to a slow, oxidative phenotype with type I myosin heavy chain expression. Using a conditional and temporally regulated Cre strategy as well as Mapk1 (ERK2) and Mapk3 (ERK1) genetically targeted mice, MEK1-ERK2 signaling was shown to underlie this fast-to-slow fiber type switching in adult skeletal muscle as well as during development. Physiologic assessment of these activated MEK1-ERK1/2 mice showed enhanced metabolic activity and oxygen consumption with greater muscle fatigue resistance. Moreover, induction of MEK1-ERK1/2 signaling increased dystrophin and utrophin protein expression in a mouse model of limb-girdle muscle dystrophy and protected myofibers from damage. In summary, sustained MEK1-ERK1/2 activity in skeletal muscle produces a fast-to-slow fiber-type switch that protects from muscular dystrophy, suggesting a therapeutic approach to enhance the metabolic effectiveness of muscle and protect from dystrophic disease.
    MeSH term(s) Animals ; Disease Models, Animal ; Dystrophin/metabolism ; MAP Kinase Kinase 1/genetics ; MAP Kinase Signaling System/genetics ; Mice ; Mitogen-Activated Protein Kinase 1/genetics ; Mitogen-Activated Protein Kinase 3/genetics ; Muscle Fatigue/genetics ; Muscle Fibers, Fast-Twitch/metabolism ; Muscle Fibers, Slow-Twitch/metabolism ; Muscle, Skeletal/metabolism ; Muscular Dystrophies, Limb-Girdle/genetics ; Muscular Dystrophies, Limb-Girdle/metabolism ; Muscular Dystrophies, Limb-Girdle/physiopathology ; Oxygen Consumption/genetics ; Severity of Illness Index ; Utrophin/metabolism
    Chemical Substances Dystrophin ; Utrophin ; Mapk1 protein, mouse (EC 2.7.11.24) ; Mapk3 protein, mouse (EC 2.7.11.24) ; Mitogen-Activated Protein Kinase 1 (EC 2.7.11.24) ; Mitogen-Activated Protein Kinase 3 (EC 2.7.11.24) ; MAP Kinase Kinase 1 (EC 2.7.12.2) ; Map2k1 protein, mouse (EC 2.7.12.2)
    Language English
    Publishing date 2019-04-09
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ISSN 2379-3708
    ISSN (online) 2379-3708
    DOI 10.1172/jci.insight.127356
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Thbs1 induces lethal cardiac atrophy through PERK-ATF4 regulated autophagy.

    Vanhoutte, Davy / Schips, Tobias G / Vo, Alexander / Grimes, Kelly M / Baldwin, Tanya A / Brody, Matthew J / Accornero, Federica / Sargent, Michelle A / Molkentin, Jeffery D

    Nature communications

    2021  Volume 12, Issue 1, Page(s) 3928

    Abstract: The thrombospondin (Thbs) family of secreted matricellular proteins are stress- and injury-induced mediators of cellular attachment dynamics and extracellular matrix protein production. Here we show that Thbs1, but not Thbs2, Thbs3 or Thbs4, induces ... ...

    Abstract The thrombospondin (Thbs) family of secreted matricellular proteins are stress- and injury-induced mediators of cellular attachment dynamics and extracellular matrix protein production. Here we show that Thbs1, but not Thbs2, Thbs3 or Thbs4, induces lethal cardiac atrophy when overexpressed. Mechanistically, Thbs1 binds and activates the endoplasmic reticulum stress effector PERK, inducing its downstream transcription factor ATF4 and causing lethal autophagy-mediated cardiac atrophy. Antithetically, Thbs1
    MeSH term(s) Activating Transcription Factor 4/genetics ; Activating Transcription Factor 4/metabolism ; Animals ; Atrophy ; Autophagy/physiology ; Cardiomegaly/genetics ; Cardiomegaly/pathology ; Endoplasmic Reticulum Stress/genetics ; Eukaryotic Initiation Factor-2/metabolism ; Gene Expression ; Lysosomes/metabolism ; Male ; Mice, Transgenic ; Myocardium/pathology ; Myocytes, Cardiac/pathology ; Proteolysis ; Thrombospondins/genetics ; Thrombospondins/metabolism ; eIF-2 Kinase/genetics ; eIF-2 Kinase/metabolism
    Chemical Substances Atf4 protein, mouse ; Eukaryotic Initiation Factor-2 ; Thrombospondins ; thrombospondin 2 ; Activating Transcription Factor 4 (145891-90-3) ; PERK kinase (EC 2.7.11.1) ; eIF-2 Kinase (EC 2.7.11.1)
    Language English
    Publishing date 2021-06-24
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; 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/s41467-021-24215-4
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Inhibition of mitochondrial permeability transition by deletion of the ANT family and CypD.

    Karch, Jason / Bround, Michael J / Khalil, Hadi / Sargent, Michelle A / Latchman, Nadina / Terada, Naohiro / Peixoto, Pablo M / Molkentin, Jeffery D

    Science advances

    2019  Volume 5, Issue 8, Page(s) eaaw4597

    Abstract: The mitochondrial permeability transition pore (MPTP) has resisted molecular identification. The original model of the MPTP that proposed the adenine nucleotide translocator (ANT) as the inner membrane pore-forming component was challenged when ... ...

    Abstract The mitochondrial permeability transition pore (MPTP) has resisted molecular identification. The original model of the MPTP that proposed the adenine nucleotide translocator (ANT) as the inner membrane pore-forming component was challenged when mitochondria from Ant1/2 double null mouse liver still had MPTP activity. Because mice express three
    MeSH term(s) Adenine Nucleotides/genetics ; Animals ; Cells, Cultured ; Peptidyl-Prolyl Isomerase F/genetics ; Female ; Male ; Mice ; Mice, Knockout ; Mitochondria/genetics ; Mitochondrial Membrane Transport Proteins/genetics ; Mitochondrial Permeability Transition Pore ; Mitochondrial Transmembrane Permeability-Driven Necrosis/genetics ; Sequence Deletion/genetics
    Chemical Substances Adenine Nucleotides ; Peptidyl-Prolyl Isomerase F ; Mitochondrial Membrane Transport Proteins ; Mitochondrial Permeability Transition Pore
    Language English
    Publishing date 2019-08-28
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2810933-8
    ISSN 2375-2548 ; 2375-2548
    ISSN (online) 2375-2548
    ISSN 2375-2548
    DOI 10.1126/sciadv.aaw4597
    Database MEDical Literature Analysis and Retrieval System OnLINE

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