ArticleCirculation research2015
Angiotensin II Induces Skeletal Muscle Atrophy by Activating TFEB-Mediated MuRF1 Expression.
Article in Circulation research, 2015. 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, 89 citations in OpenAlex.
- Trial
- Sustained alternate-day fasting potentiates doxorubicin cardiotoxicity.Cell metabolism · 2023Trial
- Trial
- Azilsartan ameliorates angiotensin II-induced skeletal muscle atrophy via AT1R-mediated PI3K/AKT/FOXO3a signaling pathway.Journal of geriatric cardiology : JGC · 2026Article
- Ubiquitin Ligases in pro-atrophic and antiatrophic signaling cascades in muscles.Molecular biology reports · 2026Review
- Deubiquitinase YOD1 Inhibition Suppresses DEX- and Denervation-Induced Muscle Atrophy Through MAFbx Destabilization.Journal of cachexia, sarcopenia and muscle · 2026Article
- Glucocorticoid-Mediated Skeletal Muscle Atrophy: Molecular Mechanisms and Potential Therapeutic Targets.International journal of molecular sciences · 2025Review
- Piezo1 channels enhance anabolic signaling activation induced by electrical stimulation of cultured myotubes.FEBS open bio · 2025Article
- Renin angiotensin system-induced muscle wasting: putative mechanisms and implications for clinicians.Molecular and cellular biochemistry · 2025Review
- Article
- Pathophysiology of Diet-Induced Acid Stress.International journal of molecular sciences · 2024Review
- Targeting Epigenetic Regulators with HDAC and BET Inhibitors to Modulate Muscle Wasting.International journal of molecular sciences · 2023Review
- Skeletal muscle atrophy, regeneration, and dysfunction in heart failure: Impact of exercise training.Journal of sport and health science · 2023Review
- Is the anti-aging effect of ACE2 due to its role in the renin-angiotensin system?-Findings from a comparison of the aging phenotypes of ACE2-deficient, Tsukuba hypertensive, and Mas-deficient mice.Hypertension research : official journal of the Japanese Society of Hypertension · 2023Review
- Oligonucleotide Therapeutics for Age-Related Musculoskeletal Disorders: Successes and Challenges.Pharmaceutics · 2023Review
- Genome Editing to Abrogate Muscle Atrophy.Advances in experimental medicine and biology · 2023Review
- Metabolic remodeling in cardiac hypertrophy and heart failure with reduced ejection fraction occurs independent of transcription factor EB in mice.Frontiers in cardiovascular medicine · 2023Article
- Transcription factor EB as a key molecular factor in human health and its implication in diseases.SAGE open medicine · 2023Review
- Targeting the Autophagy-Lysosome Pathway in a Pathophysiologically Relevant Murine Model of Reversible Heart Failure.JACC. Basic to translational science · 2022Article
- Exercise attenuates angiotensinⅡ-induced muscle atrophy by targeting PPARγ/miR-29b.Journal of sport and health science · 2022Article
2 more citing papers are in PubMed but not listed here.
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
rationaleSkeletal muscle wasting with accompanying cachexia is a life threatening complication in congestive heart failure. The molecular mechanisms are imperfectly understood, although an activated renin-angiotensin aldosterone system has been implicated. Angiotensin (Ang) II induces skeletal muscle atrophy in part by increased muscle-enriched E3 ubiquitin ligase muscle RING-finger-1 (MuRF1) expression, which may involve protein kinase D1 (PKD1).
objectiveTo elucidate the molecular mechanism of Ang II-induced skeletal muscle wasting. METHODS AND
resultsA cDNA expression screen identified the lysosomal hydrolase-coordinating transcription factor EB (TFEB) as novel regulator of the human MuRF1 promoter. TFEB played a key role in regulating Ang II-induced skeletal muscle atrophy by transcriptional control of MuRF1 via conserved E-box elements. Inhibiting TFEB with small interfering RNA prevented Ang II-induced MuRF1 expression and atrophy. The histone deacetylase-5 (HDAC5), which was directly bound to and colocalized with TFEB, inhibited TFEB-induced MuRF1 expression. The inhibition of TFEB by HDAC5 was reversed by PKD1, which was associated with HDAC5 and mediated its nuclear export. Mice lacking PKD1 in skeletal myocytes were resistant to Ang II-induced muscle wasting.
conclusionWe propose that elevated Ang II serum concentrations, as occur in patients with congestive heart failure, could activate the PKD1/HDAC5/TFEB/MuRF1 pathway to induce skeletal muscle wasting.
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