Shifts in macrophage phenotypes and macrophage competition for arginine metabolism affect the severity of muscle pathology in muscular dystrophy.
about
CCAAT-enhancer-binding protein-beta expression in vivo is associated with muscle strengthAutomated drug screening with contractile muscle tissue engineered from dystrophic myoblastsQuantitative analysis of cellular inflammation after traumatic spinal cord injury: evidence for a multiphasic inflammatory response in the acute to chronic environmentImmune Cells and Inflammation in Diabetic NephropathyAdvancements in stem cells treatment of skeletal muscle wastingExtrinsic and intrinsic control of macrophage inflammatory responsesAnti-inflammatory drugs for Duchenne muscular dystrophy: focus on skeletal muscle-releasing factorsNutraceuticals and Their Potential to Treat Duchenne Muscular Dystrophy: Separating the Credible from the ConjectureThe ischemic environment drives microglia and macrophage functionPhysical activity and the endocannabinoid system: an overviewP2RX7 purinoceptor: a therapeutic target for ameliorating the symptoms of duchenne muscular dystrophyBone marrow transplantation in dysferlin-deficient mice results in a mild functional improvement.Arginine metabolism by macrophages promotes cardiac and muscle fibrosis in mdx muscular dystrophy.CD13 regulates anchorage and differentiation of the skeletal muscle satellite stem cell population in ischemic injury.Influence of immune responses in gene/stem cell therapies for muscular dystrophies.Therapeutic potential of proteasome inhibition in Duchenne and Becker muscular dystrophiesDynamic, M2-like remodeling phenotypes of CD11c+ adipose tissue macrophages during high-fat diet--induced obesity in mice.Regulatory interactions between muscle and the immune system during muscle regenerationInflammasome up-regulation and activation in dysferlin-deficient skeletal muscle.Green tea extract decreases muscle pathology and NF-kappaB immunostaining in regenerating muscle fibers of mdx mice.Stem cell transplantation for muscular dystrophy: the challenge of immune response.CD206-positive M2 macrophages that express heme oxygenase-1 protect against diabetic gastroparesis in mice.iNOS ablation does not improve specific force of the extensor digitorum longus muscle in dystrophin-deficient mdx4cv mice.Long-term administration of the TNF blocking drug Remicade (cV1q) to mdx mice reduces skeletal and cardiac muscle fibrosis, but negatively impacts cardiac functionNeuronal nitric oxide synthase-rescue of dystrophin/utrophin double knockout mice does not require nNOS localization to the cell membraneAssociation of low numbers of CD206-positive cells with loss of ICC in the gastric body of patients with diabetic gastroparesis.IL-6 signaling blockade increases inflammation but does not affect muscle function in the mdx mouse.Asynchronous remodeling is a driver of failed regeneration in Duchenne muscular dystrophy.Macrophages improve survival, proliferation and migration of engrafted myogenic precursor cells into MDX skeletal muscleInterleukin-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.Skeletal muscle cells express ICAM-1 after muscle overload and ICAM-1 contributes to the ensuing hypertrophic response.Loss of the inducible Hsp70 delays the inflammatory response to skeletal muscle injury and severely impairs muscle regenerationEffects of hyperbaric oxygen at 1.25 atmospheres absolute with normal air on macrophage number and infiltration during rat skeletal muscle regeneration.The proton pump inhibitor lansoprazole improves the skeletal phenotype in dystrophin deficient mdx miceAdeno-associated viral (AAV) vectors do not efficiently target muscle satellite cellsMatrix metalloproteinase-9 inhibition improves proliferation and engraftment of myogenic cells in dystrophic muscle of mdx miceExtraocular muscle satellite cells are high performance myo-engines retaining efficient regenerative capacity in dystrophin deficiency.Silencing collapsin response mediator protein-2 reprograms macrophage phenotype and improves infarct healing in experimental myocardial infarction modelFibrosis and inflammation are greater in muscles of beta-sarcoglycan-null mouse than mdx mouse.
P2860
Q24620519-8C556E4F-C297-4036-AE4E-6CDAFE3FE694Q24629251-9E6FAF71-5D0D-4BF3-9B83-10640DD65F0EQ24633514-4A3BE279-DB09-4386-9D2B-DBB3A8EE4FA8Q26772998-95A6B0F3-8603-400F-B39D-06FA70E0D161Q26822437-E243A4E4-D4BD-4E26-AE54-CA3D4FCC8F6AQ26822651-B3F18584-5C46-4854-A276-14012FC71977Q28069464-B1548347-BB81-456E-B8AB-3BAA8886D596Q28072269-FEACB456-D891-4430-A56E-309A0B84411FQ28086874-4339CCF9-0767-462E-A5DB-DBB21B49E2EBQ28307668-54D96B1F-9579-44D7-B8B8-3635CC6DA7EFQ28550201-568653B5-1252-4AFC-B498-25B333D8A289Q30552419-D7AB5D98-A09B-4C0C-BC08-4A1965C00E79Q33588636-99BBC14A-227A-43F3-9D1D-25B916076001Q33680416-2DA6F9BC-E6AC-44A0-9DC8-BA96AB8C296FQ33736192-A38BB3A9-50A2-4E9D-8B76-4A951B8AF8A5Q33745227-5D9ECFD7-6E5C-47EE-95E0-B33ADB9C3816Q33803444-30802A75-CB3A-4B2F-96F8-B57ADF7BCDF8Q33841066-3A5A3A2C-ECD2-4856-B324-825AC1373718Q33882512-FFF9C76F-6813-4B62-8CDC-E9325D8A9296Q33901041-C04A7ED7-DC24-4DC6-8DC9-07DBDC46AD2CQ33902416-0C10A842-00C2-4F5E-B9A2-C5173D179764Q33905932-BB6A1F3F-EFA5-49E4-B0AA-955BC1920B97Q33955159-43B83B83-D72A-42B5-9EB3-904731B073A8Q34005353-38DCEBFD-56CE-41AE-915E-73A82ABEECB3Q34049251-616E01B1-DE9C-4B11-9638-6FC56E268B5CQ34111465-78F95108-EB43-4757-912E-4538F081A0BBQ34310898-DD12175C-491F-4145-A291-E3429DE9C470Q34332718-B5457438-ED85-4059-9CEB-E599E3EBDAE1Q34441894-389C9464-7BF2-4D14-948D-AEBB8C3DA0C7Q34505654-9FFBD3B0-9336-4D79-B127-3E9F4E6D4493Q34542698-FF735F39-0EFE-4BB7-AEBA-18B5597BE1D0Q34625853-043B6DBF-ED6E-4BEA-B8FE-8254795AFEF3Q34693368-3B631956-3961-4893-84E8-5ACD6F537ED6Q34757832-94012806-26F1-470D-8C1D-663F9BD0AECCQ34812217-4526FD38-B900-4A5C-AF74-87E6720EE122Q34886209-8BE64855-89B7-4EA3-8395-6E7C4CBC29B5Q34973330-3E518811-3FC4-44BE-80D8-0444499F6A32Q35023888-DB11D012-D427-4454-AC95-6A60D486D191Q35083493-FED88462-529A-4338-BA53-A5EC55164537Q35145764-325BCD8B-1B21-4AC1-82AC-FC2ABA9ADAFB
P2860
Shifts in macrophage phenotypes and macrophage competition for arginine metabolism affect the severity of muscle pathology in muscular dystrophy.
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-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
2008年學術文章
@zh-hant
name
Shifts in macrophage phenotype ...... thology in muscular dystrophy.
@en
Shifts in macrophage phenotype ...... thology in muscular dystrophy.
@nl
type
label
Shifts in macrophage phenotype ...... thology in muscular dystrophy.
@en
Shifts in macrophage phenotype ...... thology in muscular dystrophy.
@nl
prefLabel
Shifts in macrophage phenotype ...... thology in muscular dystrophy.
@en
Shifts in macrophage phenotype ...... thology in muscular dystrophy.
@nl
P2093
P2860
P356
P1476
Shifts in macrophage phenotype ...... thology in muscular dystrophy.
@en
P2093
Hal X Nguyen
James G Tidball
S Armando Villalta
Tomomi Gotoh
P2860
P304
P356
10.1093/HMG/DDN376
P577
2008-11-07T00:00:00Z