ReviewAntioxidants & redox signaling2017
Reactive Oxygen Species/Nitric Oxide Mediated Inter-Organ Communication in Skeletal Muscle Wasting Diseases.
Review in Antioxidants & redox signaling, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
What it found
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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.
The trial behind it
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
32 citing papers in PubMed, 48 citations in OpenAlex.
- PasteurizedNutrients · 2024Trial
- Oxidative eustress is associated with AMPK and AKT activation, GLUT4 translocation and glucose uptake in skeletal muscle cells and fibres.Redox report : communications in free radical research · 2026Article
- Elevated circulating GDF11 and its role in age-related sarcopenia: insights from clinical, transcriptomic, andFrontiers in aging · 2026Article
- Body roundness index as a novel anthropometric predictor of sarcopenia in patients with cancer: a bicontinental cohort study across Chinese and American populations.Lipids in health and disease · 2025Article
- The Influence of Irisin on Selected Organs-The Liver, Kidneys, and Lungs: The Role of Physical Exercise.Cells · 2025Review
- Review
- Nitrosative Stress in Astronaut Skeletal Muscle in Spaceflight.Antioxidants (Basel, Switzerland) · 2024Article
- Biological sex divergence in transcriptomic profiles during the onset of hindlimb unloading-induced atrophy.American journal of physiology. Cell physiology · 2023Article
- Influence of gonadectomy on muscle health in micro- and partial-gravity environments in rats.Journal of applied physiology (Bethesda, Md. : 1985) · 2023Article
- Review
- Clinical Significance of Carnitine in the Treatment of Cancer: From Traffic to the Regulation.Oxidative medicine and cellular longevity · 2023Review
- The Credible Role of Curcumin in Oxidative Stress-Mediated Mitochondrial Dysfunction in Mammals.Biomolecules · 2022Review
- Mitochondrial aberrations during the progression of disuse atrophy differentially affect male and female mice.Journal of cachexia, sarcopenia and muscle · 2021Article
- Growth differentiation factor 11 attenuates cardiac ischemia reperfusion injury via enhancing mitochondrial biogenesis and telomerase activity.Cell death & disease · 2021Article
- Article
- Female mice may have exacerbated catabolic signalling response compared to male mice during development and progression of disuse atrophy.Journal of cachexia, sarcopenia and muscle · 2021Article
- Ubiquitin Ligases at the Heart of Skeletal Muscle Atrophy Control.Molecules (Basel, Switzerland) · 2021Review
- Myokines and Heart Failure: Challenging Role in Adverse Cardiac Remodeling, Myopathy, and Clinical Outcomes.Disease markers · 2021Review
- Autophagy and metabolism.The Kaohsiung journal of medical sciences · 2021Review
- Organ-organ communication: The liver's perspective.Theranostics · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
significanceCachexia is defined as a complex metabolic syndrome that is associated with underlying illness and a loss of muscle with or without loss of fat mass. This disease is associated with a high incidence with chronic diseases such as heart failure, cancer, chronic obstructive pulmonary disease (COPD), and acquired immunodeficiency syndrome (AIDS), among others. Since there is currently no effective treatment available, cachectic patients have a poor prognosis. Elucidation of the underlying mechanisms is, therefore, an important medical task. Recent Advances: There is accumulating evidence that the diseased organs such as heart, lung, kidney, or cancer tissue secrete soluble factors, including Angiotensin II, myostatin (growth differentiation factor 8 [GDF8]), GDF11, tumor growth factor beta (TGFβ), which act on skeletal muscle. There, they induce a set of genes called atrogenes, which, among others, induce the ubiquitin-proteasome system, leading to protein degradation. Moreover, elevated reactive oxygen species (ROS) levels due to modulation of NADPH oxidases (Nox) and mitochondrial function contribute to disease progression, which is characterized by loss of muscle mass, exercise resistance, and frailty. CRITICAL ISSUES: Although substantial progress was achieved to elucidate the pathophysiology of cachexia, effectice therapeutic strategies are urgently needed. FUTURE DIRECTIONS: With the identification of key components of the aberrant inter-organ communication leading to cachexia, studies in mice and men to inhibit ROS formation, induction of anti-oxidative superoxide dismutases, and upregulation of muscular nitric oxide (NO) formation either by pharmacological tools or by exercise are promising approaches to reduce the extent of skeletal muscle wasting. Antioxid. Redox Signal. 26, 700-717.
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Registered trials
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