ArticleSkeletal muscle2020
Expression of MuRF1 or MuRF2 is essential for the induction of skeletal muscle atrophy and dysfunction in a murine pulmonary hypertension model.
Article in Skeletal muscle, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 31 citations in OpenAlex.
- Emerging significance of E3 ubiquitin ligases and Deubiquitinases in pulmonary hypertension.Molecular medicine (Cambridge, Mass.) · 2026Review
- Beyond the Vasculature: The Emerging Role of Systemic Metabolism and Immunometabolism in Pulmonary Arterial Hypertension.International journal of molecular sciences · 2026Review
- Early post-lung transplant weight gain is associated with increased long-term recipient survival.JTCVS open · 2026Article
- Small-Molecule Targeting MuRF1 Protects Against Denervation-Induced Diaphragmatic Dysfunction: Underlying Molecular Mechanisms.Journal of cachexia, sarcopenia and muscle · 2025Article
- The Monocrotaline Model of Hypertension Leads to Cachexia in Male but Not Female Mice.Journal of cachexia, sarcopenia and muscle · 2025Article
- Structure predictions of MuRF1-UBE2 complexes identify amino acid residues governing interaction selectivity for each MuRF1-E2 pair.The FEBS journal · 2025Article
- Skeletal Muscle Pathology in Pulmonary Arterial Hypertension and Its Contribution to Exercise Intolerance.Journal of the American Heart Association · 2025Review
- Antcin K ameliorates cardiotoxin-induced skeletal muscle injury and inflammation via IL-10 regulation.International journal of biological sciences · 2025Article
- Beyond Tumors: The Pivotal Role of TRIM Proteins in Chronic Non-Tumor Lung Diseases.Journal of inflammation research · 2025Review
- Pathophysiological changes of muscle after ischemic stroke: a secondary consequence of stroke injury.Neural regeneration research · 2024Review
- Loss of MuRF1 in Duroc pigs promotes skeletal muscle hypertrophy.Transgenic research · 2023Article
- TRIM55 inhibits colorectal cancer development via enhancing protein degradation of c-Myc.Cancer medicine · 2023Article
- Small-Molecule Inhibition of MuRF1 Prevents Early Disuse-Induced Diaphragmatic Dysfunction and Atrophy.International journal of molecular sciences · 2023Article
- Locomotor and respiratory muscle abnormalities in HFrEF and HFpEF.Frontiers in cardiovascular medicine · 2023Review
- Melatonin improves muscle injury and differentiation by increasing Pax7 expression.International journal of biological sciences · 2023Article
- The Role of Muscle Ring Finger-1 (MuRF1), MuRF2, MuRF3, and Atrogin-1 on Bone Microarchitecture In Vivo.Cell biochemistry and biophysics · 2022Article
- Targeting MuRF1 by small molecules in a HFpEF rat model improves myocardial diastolic function and skeletal muscle contractility.Journal of cachexia, sarcopenia and muscle · 2022Article
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- Out of Control: The Role of the Ubiquitin Proteasome System in Skeletal Muscle during Inflammation.Biomolecules · 2021Review
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
backgroundPulmonary hypertension leads to right ventricular heart failure and ultimately to cardiac cachexia. Cardiac cachexia induces skeletal muscles atrophy and contractile dysfunction. MAFbx and MuRF1 are two key proteins that have been implicated in chronic muscle atrophy of several wasting states.
methodsMonocrotaline (MCT) was injected over eight weeks into mice to establish pulmonary hypertension as a murine model for cardiac cachexia. The effects on skeletal muscle atrophy, myofiber force, and selected muscle proteins were evaluated in wild-type (WT), MuRF1, and MuRF2-KO mice by determining muscle weights, in vitro muscle force and enzyme activities in soleus and tibialis anterior (TA) muscle.
resultsIn WT, MCT treatment induced wasting of soleus and TA mass, loss of myofiber force, and depletion of citrate synthase (CS), creatine kinase (CK), and malate dehydrogenase (MDH) (all key metabolic enzymes). This suggests that the murine MCT model is useful to mimic peripheral myopathies as found in human cardiac cachexia. In MuRF1 and MuRF2-KO mice, soleus and TA muscles were protected from atrophy, contractile dysfunction, while metabolic enzymes were not lowered in MuRF1 or MuRF2-KO mice. Furthermore, MuRF2 expression was lower in MuRF1KO mice when compared to C57BL/6 mice.
conclusionsIn addition to MuRF1, inactivation of MuRF2 also provides a potent protection from peripheral myopathy in cardiac cachexia. The protection of metabolic enzymes in both MuRF1KO and MuRF2KO mice as well as the dependence of MuRF2 expression on MuRF1 suggests intimate relationships between MuRF1 and MuRF2 during muscle atrophy signaling.
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