ArticleAmerican journal of physiology. Endocrinology and metabolism2011
Cardiac proteasome activity in muscle ring finger-1 null mice at rest and following synthetic glucocorticoid treatment.
Article in American journal of physiology. Endocrinology and metabolism, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
14 citing papers in PubMed, 17 citations in OpenAlex.
- Pharmacologic or genetic interference with atrogene signaling protects against glucocorticoid-induced musculoskeletal and cardiac disease.JCI insight · 2024Article
- Does Myocardial Atrophy Represent Anti-Arrhythmic Phenotype?Biomedicines · 2022Review
- Identification of the MuRF1 Skeletal Muscle Ubiquitylome Through Quantitative Proteomics.Function (Oxford, England) · 2021Article
- The nuclear phosphatase SCP4 regulates FoxO transcription factors during muscle wasting in chronic kidney disease.Kidney international · 2017Article
- High Levels of Serum Ubiquitin and Proteasome in a Case of HLA-B27 Uveitis.International journal of molecular sciences · 2017Article
- ROCK1 reduces mitochondrial content and irisin production in muscle suppressing adipocyte browning and impairing insulin sensitivity.Scientific reports · 2016Article
- Skeletal muscle atrophy and the E3 ubiquitin ligases MuRF1 and MAFbx/atrogin-1.American journal of physiology. Endocrinology and metabolism · 2014Review
- Muscle RING finger-1 attenuates IGF-I-dependent cardiomyocyte hypertrophy by inhibiting JNK signaling.American journal of physiology. Endocrinology and metabolism · 2014Article
- Maintenance of muscle mass and load-induced growth in Muscle RING Finger 1 null mice with age.Aging cell · 2014Article
- Chronic alcohol consumption disrupts myocardial protein balance and function in aged, but not adult, female F344 rats.American journal of physiology. Regulatory, integrative and comparative physiology · 2014Article
- Altered ubiquitin-proteasome signaling in right ventricular hypertrophy and failure.American journal of physiology. Heart and circulatory physiology · 2013Article
- Cardiac and vascular atrogin-1 mRNA expression is not associated with dexamethasone efficacy in the monocrotaline model of pulmonary hypertension.Cardiovascular toxicology · 2012Article
- Transcription factor FoxO1, the dominant mediator of muscle wasting in chronic kidney disease, is inhibited by microRNA-486.Kidney international · 2012Article
- Fenofibrate unexpectedly induces cardiac hypertrophy in mice lacking MuRF1.Cardiovascular pathology : the official journal of the Society for Cardiovascular PathologyArticle
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Muscle ring finger-1 (MuRF1) is a muscle-specific E3 ubiquitin ligase that has been implicated in the regulation of cardiac mass through its control of the ubiquitin proteasome system. While it has been suggested that MuRF1 is required for cardiac atrophy, a resting cardiac phenotype has not been reported in mice with a null deletion [knockout (KO)] of MuRF1. Here, we report that MuRF1 KO mice have significantly larger hearts than age-matched wild-type (WT) littermates at ≥ 6 mo of age and that loss of cardiac mass can occur in the absence of MuRF1. The objective of this study was to determine whether changes in proteasome activity were responsible for the cardiac phenotypes observed in MuRF1 KO mice. Cardiac function, architecture, and proteasome activity were analyzed at rest and following 28 days of dexamethasone (Dex) treatment in 6-mo-old WT and MuRF1 KO mice. Echocardiography demonstrated normal cardiac function in the enlarged hearts in MURF1 KO mice. At rest, heart mass and cardiomyocyte diameter were significantly greater in MuRF1 KO than in WT mice. The increase in cardiac size in MuRF1 KO mice was related to a decrease in proteasome activity and an increase in Akt signaling relative to WT mice. Dex treatment induced a significant loss of cardiac mass in MuRF1 KO, but not WT, mice. Furthermore, Dex treatment resulted in an increase in proteasome activity in KO, but a decrease in WT, mice. In contrast, Akt/mammalian target of rapamycin signaling decreased in MuRF1 KO mice and increased in WT mice in response to Dex treatment. These findings demonstrate that MuRF1 plays an important role in regulating cardiac size through alterations in protein turnover and that MuRF1 is not required to induce cardiac atrophy.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.