N-Acetylcysteine ameliorates skeletal muscle pathophysiology in mdx mice. - Wikidata - awgldk - TriplyDB

N-Acetylcysteine ameliorates skeletal muscle pathophysiology in mdx mice.

N-Acetylcysteine ameliorates skeletal muscle pathophysiology in mdx mice.

http://www.wikidata.org/entity/Q46765634

about

Current and emerging treatment strategies for Duchenne muscular dystrophy SIRT1: A Novel Target for the Treatment of Muscular Dystrophies Pre-clinical drug tests in the mdx mouse as a model of dystrophinopathies: an overview Insights into the molecular etiology of exercise-induced inflammation: opportunities for optimizing performance Anti-inflammatory drugs for Duchenne muscular dystrophy: focus on skeletal muscle-releasing factors The role of oxidative stress in skeletal muscle injury and regeneration: focus on antioxidant enzymes Dystrophic Cardiomyopathy-Potential Role of Calcium in Pathogenesis, Treatment and Novel Therapies Therapeutic targeting of signaling pathways in muscular dystrophy.Skeletal muscle NADPH oxidase is increased and triggers stretch-induced damage in the mdx mouse.Antioxidant supplement inhibits skeletal muscle constitutive autophagy rather than fasting-induced autophagy in mice.Green tea extract decreases muscle pathology and NF-kappaB immunostaining in regenerating muscle fibers of mdx mice.Mechanisms of muscle weakness in muscular dystrophy The different impact of a high fat diet on dystrophic mdx and control C57Bl/10 mice Delayed cardiomyopathy in dystrophin deficient mdx mice relies on intrinsic glutathione resource.Pharmacologic management of Duchenne muscular dystrophy: target identification and preclinical trials N-Acetylcysteine increases corneal endothelial cell survival in a mouse model of Fuchs endothelial corneal dystrophy Monoamine oxidase inhibition prevents mitochondrial dysfunction and apoptosis in myoblasts from patients with collagen VI myopathies.Diapocynin, a dimer of the NADPH oxidase inhibitor apocynin, reduces ROS production and prevents force loss in eccentrically contracting dystrophic muscle Interleukin-10 reduces the pathology of mdx muscular dystrophy by deactivating M1 macrophages and modulating macrophage phenotype.Inflammatory monocytes promote progression of Duchenne muscular dystrophy and can be therapeutically targeted via CCR2.Nε-lysine acetylation determines dissociation from GAP junctions and lateralization of connexin 43 in normal and dystrophic heart.Mitigation of muscular dystrophy in mice by SERCA overexpression in skeletal muscle.Bmi1 enhances skeletal muscle regeneration through MT1-mediated oxidative stress protection in a mouse model of dystrophinopathy.Soluble activin receptor type IIB increases forward pulling tension in the mdx mouse.Living in a box or call of the wild? Revisiting lifetime inactivity and sarcopenia IFN-γ promotes muscle damage in the mdx mouse model of Duchenne muscular dystrophy by suppressing M2 macrophage activation and inhibiting muscle cell proliferation Aquapuncture Using Stem Cell Therapy to Treat Mdx Mice.Agents Which Inhibit NF-κB Signaling Block Spontaneous Contractile Activity and Negatively Influence Survival of Developing Myotubes.A new therapeutic effect of simvastatin revealed by functional improvement in muscular dystrophy.Emerging drugs for Duchenne muscular dystrophy Absence of Dystrophin Disrupts Skeletal Muscle Signaling: Roles of Ca2+, Reactive Oxygen Species, and Nitric Oxide in the Development of Muscular Dystrophy.Sarcospan: a small protein with large potential for Duchenne muscular dystrophy Wasting mechanisms in muscular dystrophy.Leupeptin-based inhibitors do not improve the mdx phenotype.Levels of inflammation and oxidative stress, and a role for taurine in dystropathology of the Golden Retriever Muscular Dystrophy dog model for Duchenne Muscular Dystrophy.Role of dystroglycan in limiting contraction-induced injury to the sarcomeric cytoskeleton of mature skeletal muscle.Differential Expression of NADPH Oxidases Depends on Skeletal Muscle Fiber Type in Rats.Cytoglobin modulates myogenic progenitor cell viability and muscle regeneration Immune-mediated mechanisms potentially regulate the disease time-course of duchenne muscular dystrophy and provide targets for therapeutic intervention.S-nitrosation and ubiquitin-proteasome system interplay in neuromuscular disorders.

P2860

Q26741535-1C447859-0CE4-4D65-8435-6FAB662AD241 Q26748736-22410C2B-ECB4-404F-8E0E-EB77C8B36470 Q26849430-490D0570-AB6D-4E02-B439-A6FABAB62DCC Q28066359-0378103B-71CC-4FBD-AF9A-F8D66B7FDA15 Q28069464-C0C006CF-02EB-44CB-B933-CEE63F49EAEA Q28076877-A90AC7CC-14E2-412F-97DB-53BBF449D513 Q33608478-5CD55E39-8B9E-4C57-B3DD-3805574DC560 Q33707964-DA6F9E6B-B39E-4C15-B17E-8D5A3F3FF09F Q33781098-E25B7623-F775-4E89-A0BC-2B44487F8DDF Q33854662-13574316-2054-4CFC-B880-7C2A47B69549 Q33901041-C3A2B34E-2978-49BA-AB0B-324E8E4A5B70 Q33950716-DD39AC8F-9DA3-4D2C-92A0-7AA9A3E0E3B7 Q34077151-AD714968-9C89-426B-AEF7-58E2F93BDC58 Q34086953-EF0BD228-C4AE-46E0-B227-7CAAF1515884 Q34152280-E8702B70-1B17-4640-9C92-131863179EF4 Q34241870-7F65DEDE-52A8-48A7-887E-129AA932051A Q34266732-98FB28BA-BBBC-4ACD-9731-AB97F4103930 Q34444163-E95FB66E-A468-4678-9D89-312D80A5C44B Q34505654-24363462-F86F-4CB4-AD27-3C533A4E7FBC Q34542698-C124B32D-0AFF-474A-8B77-4668F90C9E91 Q34582749-E9A243C7-D9E0-4929-830D-773FC1016519 Q34627089-1E92A69E-00A3-4293-AC64-C5856DF1B252 Q34708380-9E603001-BA1C-4D36-8BFE-3A715010220F Q34786048-3F6DD123-D6A0-4B3B-9048-B2405A404CFD Q35222190-CCECBA02-64A5-407E-8658-F83D3DE5B292 Q35523128-0B685305-7671-44F2-ACD9-A917D9C745D3 Q35649642-EA3B6C2D-B5FE-438C-89E4-E0971209F827 Q35679235-13319A00-59E3-471D-B7A9-60D3A82ECCD6 Q36179162-7C79E3C2-84FF-4E6E-AEE3-C93F98D16CDA Q36363716-3309F67B-EA8C-4E64-B70C-8A01F8063AF1 Q36422465-A33F14D1-D4B2-4A28-BBC5-26A799AFB2E3 Q36690397-1A5132B4-E7AE-4746-B59D-4A2F820FE363 Q37138490-B648A2E4-3A13-40D2-A7F6-4FF94A873B70 Q37174711-D18A6ADC-9177-4957-9BF0-B05C13714B72 Q37246026-5A3F702C-91B0-4ACB-A483-309CA1D83D97 Q37304803-BA8E9922-3820-48CF-8611-F0DC99DD4EBD Q37402362-A0285903-3667-42B3-BCC7-785B00EA9055 Q37474956-DBB69129-7AF4-49F2-9756-653D975778F9 Q37583167-E09ED025-56BC-4D49-BD5B-3CEB535A1ACD Q37592652-F2248949-450D-4711-9F3C-D8C2ED4DA6A9

P2860

N-Acetylcysteine ameliorates skeletal muscle pathophysiology in mdx mice.

http://www.wikidata.org/entity/Q46765634

description

2008 nî lūn-bûn

@nan

2008年の論文

@ja

2008年学术文章

@wuu

2008年学术文章

@zh

2008年学术文章

@zh-cn

2008年学术文章

@zh-hans

2008年学术文章

@zh-my

2008年学术文章

@zh-sg

2008年學術文章

@yue

2008年學術文章

@zh-hant

name

N-Acetylcysteine ameliorates skeletal muscle pathophysiology in mdx mice.

@en

N-Acetylcysteine ameliorates skeletal muscle pathophysiology in mdx mice.

@nl

type

label

N-Acetylcysteine ameliorates skeletal muscle pathophysiology in mdx mice.

@en

N-Acetylcysteine ameliorates skeletal muscle pathophysiology in mdx mice.

@nl

prefLabel

N-Acetylcysteine ameliorates skeletal muscle pathophysiology in mdx mice.

@en

N-Acetylcysteine ameliorates skeletal muscle pathophysiology in mdx mice.

@nl

P1433

Q46765634-2D030181-0147-4FF2-91B4-1667DB5146B3

P1476

Q46765634-C2AE7ECF-C62C-49FF-8FC6-F08981248EE7

P2093

Q46765634-05D343E9-FB7E-4A5B-BB9A-BA69601372A7

Q46765634-23BFAC66-F492-4A45-A248-C2167083F321

Q46765634-B84B36E2-3348-4B26-A6F5-66F07297FB0F

P2860

Q46765634-07B35A3A-A7BA-444A-9DDE-491FB8DBC329

Q46765634-09E8A368-BF75-44F7-BD11-924D5478CBD0

Q46765634-15269EE5-6969-464B-B4E2-B378B3195F50

Q46765634-18363312-D646-46B0-8DE7-7C7A2087CA56

Q46765634-2530EB71-7E03-4F50-83A2-A2E825D3EC50

Q46765634-303AAE3E-F355-468C-90C9-73CBF1EB4801

Q46765634-320E37B6-F021-404E-B78F-F12A0D6657CF

Q46765634-32F1F4BD-E3ED-445A-BE73-581E58FBAC6F

Q46765634-3399A64E-F202-4622-9D4E-76D56AA80F49

Q46765634-3960260D-937B-4E4F-B5AC-57938E98AA1B

P304

Q46765634-ECDD1A4E-8D81-49A7-8896-CBBC755CC67E

P31

Q46765634-9A6AD7F3-4B24-4E91-9FE3-C7CBA8FFFE68

P356

Q46765634-F77E7CEF-F1D7-45A0-A829-4698C03C8B18

P407

Q46765634-28ABACD0-68B1-4305-94DE-226D35FA1023

P433

Q46765634-1823CCDD-6A2B-4AB3-AE65-A00024A05B12

P478

Q46765634-999BD4A0-AC1B-4F43-AF72-B16DA325C217

P50

Q46765634-0190477A-6BEF-43B7-8B11-3EB12FF81A7E

P577

Q46765634-1E080BA6-631F-4885-882F-94A25312D5C9

P5875

Q46765634-981A113A-69CE-4C69-9D8C-14385B0A6C91

P698

Q46765634-6FF0E842-3736-4CA9-B9D8-73D9494601CC

P921

Q46765634-169C93B3-819F-477B-86F2-8D1600DE1245

P932

Q46765634-D36038D4-D299-444D-90C0-EBAA52B1DC9A

P356

JPHYSIOL.2007.148338

P1433

The Journal of Physiology

P1476

N-Acetylcysteine ameliorates skeletal muscle pathophysiology in mdx mice.

@en

P2093

Catherine Pham

http://www.w3.org/2001/XMLSchema#string

Nicholas P Whitehead

http://www.w3.org/2001/XMLSchema#string

Othon L Gervasio

http://www.w3.org/2001/XMLSchema#string

P2860

Caveolin-3 directly interacts with the C-terminal tail of beta -dystroglycan. Identification of a central WW-like domain within caveolin family members

Effects of dietary curcumin or N-acetylcysteine on NF-kappaB activity and contractile performance in ambulatory and unloaded murine soleus

Dystrophin: the protein product of the Duchenne muscular dystrophy locus

Calcium, ATP, and ROS: a mitochondrial love-hate triangle

The WW domain: linking cell signalling to the membrane cytoskeleton.

Alteration in calcium handling at the subcellular level in mdx myotubes.

Early events in stretch-induced muscle damage.

Invited Review: redox modulation of skeletal muscle contraction: what we know and what we don't.

Oxidative stress and the pathogenesis of muscular dystrophies.

Selective fluorescent imaging of superoxide in vivo using ethidium-based probes.

P304

2003-2014

http://www.w3.org/2001/XMLSchema#string

P31

scholarly article

P356

10.1113/JPHYSIOL.2007.148338

http://www.w3.org/2001/XMLSchema#string

P407

P433

7

http://www.w3.org/2001/XMLSchema#string

P478

586

http://www.w3.org/2001/XMLSchema#string

P50

P577

2008-02-07T00:00:00Z

http://www.w3.org/2001/XMLSchema#dateTime

P5875

5592887

http://www.w3.org/2001/XMLSchema#string

P698

18258657

http://www.w3.org/2001/XMLSchema#string

P921

pathophysiology

P932

2375717

http://www.w3.org/2001/XMLSchema#string