Deletion of periostin reduces muscular dystrophy and fibrosis in mice by modulating the transforming growth factor-β pathway. - Wikidata - awgldk - TriplyDB

Deletion of periostin reduces muscular dystrophy and fibrosis in mice by modulating the transforming growth factor-β pathway.

Deletion of periostin reduces muscular dystrophy and fibrosis in mice by modulating the transforming growth factor-β pathway.

http://www.wikidata.org/entity/Q36079434

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The role of fibrosis in Duchenne muscular dystrophy Inhibition of the Unfolded Protein Response Mechanism Prevents Cardiac Fibrosis A mouse model for dominant collagen VI disorders: heterozygous deletion of Col6a3 Exon 16 Inhibition of TGF-β signaling in mesenchymal stem cells of subchondral bone attenuates osteoarthritis Genetic lineage tracing defines myofibroblast origin and function in the injured heart.Inhibition of periostin expression protects against the development of renal inflammation and fibrosis.P38α MAPK underlies muscular dystrophy and myofiber death through a Bax-dependent mechanism.A novel immunomodulator, FTY-720 reverses existing cardiac hypertrophy and fibrosis from pressure overload by targeting NFAT (nuclear factor of activated T-cells) signaling and periostin.Chronic oral administration of Ang-(1-7) improves skeletal muscle, autonomic and locomotor phenotypes in muscular dystrophy.Identification of a conserved set of upregulated genes in mouse skeletal muscle hypertrophy and regrowth Quantitative proteomic analysis reveals metabolic alterations, calcium dysregulation, and increased expression of extracellular matrix proteins in laminin α2 chain-deficient muscle.Resveratrol ameliorates myocardial fibrosis by inhibiting ROS/ERK/TGF-β/periostin pathway in STZ-induced diabetic mice.Possible involvement of TGF-β/periostin in fibrosis of right atrial appendages in patients with atrial fibrillation ALS skeletal muscle shows enhanced TGF-β signaling, fibrosis and induction of fibro/adipogenic progenitor markers.Deletion of Periostin Protects Against Atherosclerosis in Mice by Altering Inflammation and Extracellular Matrix Remodeling Collagen VI deficiency reduces muscle pathology, but does not improve muscle function, in the γ-sarcoglycan-null mouse Modifying muscular dystrophy through transforming growth factor-β.Wasting mechanisms in muscular dystrophy.Coronary adventitial cells are linked to perivascular cardiac fibrosis via TGFβ1 signaling in the mdx mouse model of Duchenne muscular dystrophy.Integrating the myocardial matrix into heart failure recognition and management.Wnt protein-mediated satellite cell conversion in adult and aged mice following voluntary wheel running.Periostin promotes renal cyst growth and interstitial fibrosis in polycystic kidney disease.Extrinsic Regulation of Satellite Cell Function and Muscle Regeneration Capacity during Aging.Pathoproteomic profiling of the skeletal muscle matrisome in dystrophinopathy associated myofibrosis.A healthy tension in translational research.Periostin promotes hepatic fibrosis in mice by modulating hepatic stellate cell activation via αv integrin interaction.IGF-1/GH axis enhances losartan treatment in Lama2-related muscular dystrophy.Blockade of PDGF Receptors by Crenolanib Has Therapeutic Effect in Patient Fibroblasts and in Preclinical Models of Systemic Sclerosis.Periostin as a multifunctional modulator of the wound healing response.Label-free mass spectrometric analysis of the mdx-4cv diaphragm identifies the matricellular protein periostin as a potential factor involved in dystrophinopathy-related fibrosis.Outside in: The matrix as a modifier of muscular dystrophy.TGFBI functions similar to periostin but is uniquely dispensable during cardiac injury Laminin-111 improves muscle repair in a mouse model of merosin-deficient congenital muscular dystrophy.Elastase levels and activity are increased in dystrophic muscle and impair myoblast cell survival, proliferation and differentiation.Three distinct cell populations express extracellular matrix proteins and increase in number during skeletal muscle fibrosis.Dysregulation of matricellular proteins is an early signature of pathology in laminin-deficient muscular dystrophy.Cardiac fibroblast glycogen synthase kinase-3β regulates ventricular remodeling and dysfunction in ischemic heart.Periostin and its interacting proteins in the construction of extracellular architectures.Periostin in kidney diseases.Specialized fibroblast differentiated states underlie scar formation in the infarcted mouse heart.

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P2860

Deletion of periostin reduces muscular dystrophy and fibrosis in mice by modulating the transforming growth factor-β pathway.

http://www.wikidata.org/entity/Q36079434

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Deletion of periostin reduces ...... rming growth factor-β pathway.

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

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Deletion of periostin reduces ...... rming growth factor-β pathway.

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Angela Lorts

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Elizabeth M McNally

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Troy A Baudino

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P2860

Identification and characterization of a novel protein, periostin, with restricted expression to periosteum and periodontal ligament and increased expression by transforming growth factor beta

Periostin as a novel factor responsible for ventricular dilation

The extracellular matrix: not just pretty fibrils

Roles of epithelial cell-derived periostin in TGF-beta activation, collagen production, and collagen gel elasticity in asthma.

A web-accessible complete transcriptome of normal human and DMD muscle.

Periostin promotes invasiveness and resistance of pancreatic cancer cells to hypoxia-induced cell death: role of the beta4 integrin and the PI3k pathway.

Angiotensin II type 1 receptor blockade attenuates TGF-beta-induced failure of muscle regeneration in multiple myopathic states.

Periostin regulates collagen fibrillogenesis and the biomechanical properties of connective tissues.

Regulation of myogenic differentiation by type beta transforming growth factor.

Periostin is essential for cardiac healing after acute myocardial infarction.

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