NF-κB activation is required for the transition of pulmonary inflammation to muscle atrophy.
about
Cachexia in chronic obstructive pulmonary disease: new insights and therapeutic perspectiveThe mechanisms of cachexia underlying muscle dysfunction in COPDLeucine and HMB differentially modulate proteasome system in skeletal muscle under different sarcopenic conditionsQuantitative computed tomography measures of pectoralis muscle area and disease severity in chronic obstructive pulmonary disease. A cross-sectional studyRole of IGF-I and the TNFα/NF-κB pathway in the induction of muscle atrogenes by acute inflammation.Nutrition and respiratory health--feature review.A conceptual framework: the early and late phases of skeletal muscle dysfunction in the acute respiratory distress syndrome.Therapeutic exercise attenuates neutrophilic lung injury and skeletal muscle wasting.Impaired exercise capacity and skeletal muscle function in a mouse model of pulmonary inflammation.Ubiquitin E3 ligase Wwp1 negatively regulates osteoblast function by inhibiting osteoblast differentiation and migrationThe posterior cricoarytenoid muscle is spared from MuRF1-mediated muscle atrophy in mice with acute lung injury.Cathepsin G degradation of phospholipid transfer protein (PLTP) augments pulmonary inflammation.Nuclear factor-κB signalling and transcriptional regulation in skeletal muscle atrophy.Mechanisms underlying the anti-wasting effect of L-carnitine supplementation under pathologic conditions: evidence from experimental and clinical studies.Signaling pathways controlling skeletal muscle massMechanisms modulating skeletal muscle phenotype.Phase II drugs that are currently in development for the treatment of cachexia.Lung injury-induced skeletal muscle wasting in aged mice is linked to alterations in long chain fatty acid metabolismPharmacological inhibition of GSK-3 in a guinea pig model of LPS-induced pulmonary inflammation: II. Effects on skeletal muscle atrophy.Exposure to cigarette smoke induces overexpression of von Hippel-Lindau tumor suppressor in mouse skeletal muscle.Differential regulation of muscle protein turnover in response to emphysema and acute pulmonary inflammation.CAT-2003: A novel sterol regulatory element-binding protein inhibitor that reduces steatohepatitis, plasma lipids, and atherosclerosis in apolipoprotein E*3-Leiden mice.Pulmonary inflammation-induced loss and subsequent recovery of skeletal muscle mass require functional poly-ubiquitin conjugation.
P2860
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P2860
NF-κB activation is required for the transition of pulmonary inflammation to muscle atrophy.
description
2012 nî lūn-bûn
@nan
2012年の論文
@ja
2012年論文
@yue
2012年論文
@zh-hant
2012年論文
@zh-hk
2012年論文
@zh-mo
2012年論文
@zh-tw
2012年论文
@wuu
2012年论文
@zh
2012年论文
@zh-cn
name
NF-κB activation is required f ...... nflammation to muscle atrophy.
@en
NF-κB activation is required f ...... nflammation to muscle atrophy.
@nl
type
label
NF-κB activation is required f ...... nflammation to muscle atrophy.
@en
NF-κB activation is required f ...... nflammation to muscle atrophy.
@nl
prefLabel
NF-κB activation is required f ...... nflammation to muscle atrophy.
@en
NF-κB activation is required f ...... nflammation to muscle atrophy.
@nl
P2093
P2860
P356
P1476
NF-κB activation is required f ...... nflammation to muscle atrophy.
@en
P2093
Astrid Haegens
Chad Steele
Harald Carlsen
Juanita H J Vernooy
Menno P J de Winther
Ramon C J Langen
Steven E Shoelson
P2860
P304
P356
10.1165/RCMB.2011-0119OC
P577
2012-04-26T00:00:00Z