ArticleBritish journal of cancer2005
Angiotensin II directly induces muscle protein catabolism through the ubiquitin-proteasome proteolytic pathway and may play a role in cancer cachexia.
Article in British journal of cancer, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers, 1 of them a synthesis that pooled it.
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
69 citing papers in PubMed, 1 synthesis or guideline pooled it, 140 citations in OpenAlex.
- MASLD and sarcopenia research (2012-2025): a multi-database bibliometric analysis.Frontiers in nutrition · 2026Pooled it
- The Effect of ACE Inhibitor on the Quality of Life amongst Patients with Cancer Cachexia.Asian Pacific journal of cancer prevention : APJCP · 2020Trial
- Review
- Angiotensin II Type 1 Receptor Blocker Usage Prevents Oxidative Stress and Muscle Dysfunction in HIV.Fundamental & clinical pharmacology · 2025Article
- Renin angiotensin system-induced muscle wasting: putative mechanisms and implications for clinicians.Molecular and cellular biochemistry · 2025Review
- Article
- Deciphering molecular crosstalk mechanisms between skeletal muscle atrophy and KRAS-mutant pancreatic cancer: a literature review.Hepatobiliary surgery and nutrition · 2025Review
- Nutritional Status and Post-Cardiac Surgery Outcomes: An Updated Review with Emphasis on Cognitive Function.Journal of clinical medicine · 2024Review
- Withaferin A as a Potential Therapeutic Target for the Treatment of Angiotensin II-Induced Cardiac Cachexia.Cells · 2024Article
- Molecular mechanisms underlying sarcopenia in heart failure.The journal of cardiovascular aging · 2024Article
- Review
- Analysis of the association between osteoporosis and muscle strength in Korean adults: a national cross-sectional study.Journal of health, population, and nutrition · 2023Article
- A Sarcopenia Index Derived from Malnutrition Parameters in Elderly Haemodialysis Patients.Nutrients · 2023Article
- Host-Derived Cytotoxic Agents in Chronic Inflammation and Disease Progression.International journal of molecular sciences · 2023Review
- Progressive development of melanoma-induced cachexia differentially impacts organ systems in mice.Cell reports · 2023Article
- Spinal cord injury impairs cardiac function due to impaired bulbospinal sympathetic control.Nature communications · 2022Article
- Cancer cachexia as a multiorgan failure: Reconstruction of the crime scene.Frontiers in cell and developmental biology · 2022Review
- Shared and distinct mechanisms of skeletal muscle atrophy: A narrative review.Ageing research reviews · 2021Review
- Ubiquitin Ligases at the Heart of Skeletal Muscle Atrophy Control.Molecules (Basel, Switzerland) · 2021Review
- Molecular and Biomechanical Adaptations to Mechanical Stretch in Cultured Myotubes.Frontiers in physiology · 2021Review
9 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The ability of angiotensin I (Ang I) and II (Ang II) to induce directly protein degradation in skeletal muscle has been studied in murine myotubes. Angiotensin I stimulated protein degradation with a parabolic dose-response curve and with a maximal effect between 0.05 and 0.1 microM. The effect was attenuated by coincubation with the angiotensin-converting enzyme (ACE) inhibitor imidaprilat, suggesting that angiotensin I stimulated protein degradation through conversion to Ang II. Angiotensin II also stimulated protein breakdown with a similar dose-response curve, and with a maximal effect between 1 and 2.5 microM. Total protein degradation, induced by both Ang I and Ang II, was attenuated by the proteasome inhibitors lactacystin (5 microM) and MG132 (10 microM), suggesting that the effect was mediated through upregulation of the ubiquitin-proteasome proteolytic pathway. Both Ang I and Ang II stimulated an increased proteasome 'chymotrypsin-like' enzyme activity as well as an increase in protein expression of 20S proteasome alpha-subunits, the 19S subunits MSS1 and p42, at the same concentrations as those inducing protein degradation. The effect of Ang I was attenuated by imidaprilat, confirming that it arose from conversion to Ang II. These results suggest that Ang II stimulates protein degradation in myotubes through induction of the ubiquitin-proteasome pathway. Protein degradation induced by Ang II was inhibited by insulin-like growth factor and by the polyunsaturated fatty acid, eicosapentaenoic acid. These results suggest that Ang II has the potential to cause muscle atrophy through an increase in protein degradation. The highly lipophilic ACE inhibitor imidapril (Vitortrade mark) (30 mg kg(-1)) attenuated the development of weight loss in mice bearing the MAC16 tumour, suggesting that Ang II may play a role in the development of cachexia in this model.
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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.