ArticleAmerican journal of respiratory and critical care medicine2012
A critical role for muscle ring finger-1 in acute lung injury-associated skeletal muscle wasting.
Article in American journal of respiratory and critical care medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.
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Who cites it
62 citing papers in PubMed.
- Therapeutic exercise attenuates neutrophilic lung injury and skeletal muscle wasting.Science translational medicine · 2015Trial
- Ubiquitin Ligases in pro-atrophic and antiatrophic signaling cascades in muscles.Molecular biology reports · 2026Review
- The flux of energy in critical illness and the obesity paradox.Physiological reviews · 2025Review
- Muscle wasting and the response to exercise in lung-injured mice is not primarily driven through the glucocorticoid axis.American journal of physiology. Endocrinology and metabolism · 2025Article
- Article
- Exercise interventions for pulmonary function impairment: rehabilitation strategies from the acute phase to long-term sequelae.Frontiers in physiology · 2025Review
- Macrophages modulate skeletal muscle wasting and recovery in acute lung injury in mice.Physiological reports · 2024Article
- Uncovering the mechanisms of MuRF1-induced ubiquitylation and revealing similarities with MuRF2 and MuRF3.Biochemistry and biophysics reports · 2024Article
- A critical discussion on the relationship between E3 ubiquitin ligases, protein degradation, and skeletal muscle wasting: it's not that simple.American journal of physiology. Cell physiology · 2023Review
- Research progress on the pathogenesis and treatment of ventilator-induced diaphragm dysfunction.Heliyon · 2023Review
- Article
- Skeletal muscle macrophage ablation in mice.Journal of immunological methods · 2022Article
- Peripheral and respiratory muscle impairment during murine acute lung injury.Physiological reports · 2022Article
- Prolonged Mechanical Ventilation: Outcomes and Management.Journal of clinical medicine · 2022Review
- Editorial: Elevated Carbon Dioxide Sensing and Physiologic Effects.Frontiers in physiology · 2022Article
- Influenza A Virus-Driven Airway Inflammation may be Dissociated From Limb Muscle Atrophy in Cigarette Smoke-Exposed Mice.Frontiers in pharmacology · 2022Article
- A narrative review of skeletal muscle atrophy in critically ill children: pathogenesis and chronic sequelae.Translational pediatrics · 2021Review
- Long-Term Outcomes in Acute Respiratory Distress Syndrome: Epidemiology, Mechanisms, and Patient Evaluation.Critical care clinics · 2021Review
- Activated mast cells in skeletal muscle can be a potential mediator for cancer-associated cachexia.Journal of cachexia, sarcopenia and muscle · 2021Article
- Aging Influences the Metabolic and Inflammatory Phenotype in an Experimental Mouse Model of Acute Lung Injury.The journals of gerontology. Series A, Biological sciences and medical sciences · 2021Article
2 more citing papers are in PubMed but not listed here.
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Authors and funding
21 authors.
Funding
Abstract
rationaleAcute lung injury (ALI) is a debilitating condition associated with severe skeletal muscle weakness that persists in humans long after lung injury has resolved. The molecular mechanisms underlying this condition are unknown.
objectivesTo identify the muscle-specific molecular mechanisms responsible for muscle wasting in a mouse model of ALI.
methodsChanges in skeletal muscle weight, fiber size, in vivo contractile performance, and expression of mRNAs and proteins encoding muscle atrophy-associated genes for muscle ring finger-1 (MuRF1) and atrogin1 were measured. Genetic inactivation of MuRF1 or electroporation-mediated transduction of miRNA-based short hairpin RNAs targeting either MuRF1 or atrogin1 were used to identify their role in ALI-associated skeletal muscle wasting. MEASUREMENTS AND MAIN
resultsMice with ALI developed profound muscle atrophy and preferential loss of muscle contractile proteins associated with reduced muscle function in vivo. Although mRNA expression of the muscle-specific ubiquitin ligases, MuRF1 and atrogin1, was increased in ALI mice, only MuRF1 protein levels were up-regulated. Consistent with these changes, suppression of MuRF1 by genetic or biochemical approaches prevented muscle fiber atrophy, whereas suppression of atrogin1 expression was without effect. Despite resolution of lung injury and down-regulation of MuRF1 and atrogin1, force generation in ALI mice remained suppressed.
conclusionsThese data show that MuRF1 is responsible for mediating muscle atrophy that occurs during the period of active lung injury in ALI mice and that, as in humans, skeletal muscle dysfunction persists despite resolution of lung injury.
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