ArticleThe American journal of the medical sciences2015
Mechanisms of Cachexia in Chronic Disease States.
Article in The American journal of the medical sciences, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 4 of them syntheses that pooled it.
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Who cites it
57 citing papers in PubMed, 4 syntheses or guidelines pooled it, 107 citations in OpenAlex.
- Recent Perspectives on the Physiological and Therapeutic Benefits of Placental Extracts in Chronic Noninfectious Diseases and Aging.Current medicinal chemistry · 2026Pooled it
- Multimodal interventions for cachexia management.The Cochrane database of systematic reviews · 2025Pooled it
- Cancer- and cardiac-induced cachexia: same fate through different inflammatory mediators?Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022Pooled it
- Neuromuscular electrical stimulation of the thighs in cardiac patients with implantable cardioverter defibrillators.Wiener klinische Wochenschrift · 2016Pooled it
- Withaferin A Attenuates Angiotensin II-Induced Right Ventricular Dysfunction and Fibrosis.International journal of molecular sciences · 2026Article
- When the Heart, Kidneys, and Body Waste Away: A Review of Cachexia in Cardiorenal Syndrome.Current heart failure reports · 2025Review
- Combating chronic kidney disease-associated cachexia: A literature review of recent therapeutic approaches.BMC nephrology · 2025Review
- Metabolic musculoskeletal disorders in patients with inflammatory bowel disease.The Korean journal of internal medicine · 2025Review
- Interaction and overall effects of underweight, low muscle mass, malnutrition, and inflammation on early-onset mild cognitive impairment in type 2 diabetes.Frontiers in aging neuroscience · 2025Article
- Mechanisms, assessment, and exercise interventions for skeletal muscle dysfunction post-chemotherapy in breast cancer: from inflammation factors to clinical practice.Frontiers in oncology · 2025Review
- Cancer cachexia: multilevel metabolic dysfunction.Nature metabolism · 2024Review
- Nutritional Status and Post-Cardiac Surgery Outcomes: An Updated Review with Emphasis on Cognitive Function.Journal of clinical medicine · 2024Review
- Testosterone replacement therapy in patients with cachexia: a contemporary review of the literature.Sexual medicine reviews · 2024Review
- Clinical Overview of Sarcopenia, Frailty, and Malnutrition in Patients With Liver Cirrhosis.Gastroenterology research · 2024Review
- Skeletal muscle dysfunctions in pulmonary arterial hypertension: Effects of aerobic exercise training.Frontiers in physiology · 2023Review
- Phase angle derived from bioelectrical impedance analysis as a marker for predicting sarcopenia.Frontiers in nutrition · 2022Review
- The Pathogenesis of End-Stage Renal Disease from the Standpoint of the Theory of General Pathological Processes of Inflammation.International journal of molecular sciences · 2021Review
- Review
- NRF2 in Cardiovascular Diseases: a Ray of Hope!Journal of cardiovascular translational research · 2021Review
- Skeletal muscle heme oxygenase-1 activity regulates aerobic capacity.Cell reports · 2021Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Sarcopenia and cachexia are muscle wasting syndromes associated with aging and with many chronic diseases, such as congestive heart failure (CHF), diabetes, cancer, chronic obstructive pulmonary disease and chronic kidney disease (CKD). While mechanisms are complex, these conditions are often accompanied by elevated angiotensin II (Ang II). Patients with advanced CHF or CKD often have increased Ang II levels and cachexia, and angiotensin-converting enzyme inhibitor treatment improves weight loss. It was found that Ang II infusion in rodents leads to skeletal muscle wasting. Ang II increases cytokines and circulating hormones, such as tumor necrosis factor-α, interleukin-6, serum amyloid-A and glucocorticoids, which regulate muscle protein synthesis and degradation. Ang II-induced muscle wasting is caused by alterations in insulin-like growth factor-1 signaling, enhanced muscle protein breakdown via the ubiquitin-proteasome system and decreased appetite resulting from the downregulation of hypothalamic orexigenic neuropeptides, such as Npy and orexin. Ang II also inhibits 5' adenosine monophosphate-activated protein kinase activity and disrupts normal energy balance via the activation of 5' adenosine monophosphate-activated protein kinase phosphatase PP2Cα. Furthermore, Ang II inhibits skeletal muscle stem (satellite) cell proliferation, leading to lowered muscle regenerative capacity. Distinct satellite cell angiotensin receptor subtypes have different effects on different stages of differentiation and are critical for the regulation of muscle regeneration. These data suggest that the renin-angiotensin system plays a critical role in mechanisms underlying cachexia in chronic disease states, and it is a promising target for the treatment of muscle atrophy in patients with diseases such as CHF and CKD.
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Registered trials
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