ArticleeLife2023
Lipid hydroperoxides promote sarcopenia through carbonyl stress.
Article in eLife, 2023. 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, 50 citations in OpenAlex.
- Selenium Deficiency is a Significant Risk Factor for Sarcopenia: Evidence and Selenoprotein-Mediated Mechanisms.Biological trace element research · 2026Review
- Ferroptosis-related stress during aging and its relevance to disease.GeroScience · 2026Review
- Iron homeostasis disruption and lipid peroxidation in skeletal muscle during short-term immobilization.FEBS open bio · 2026Article
- Age-related changes in adrenergic regulation of contractility and redox status of glycolytic and oxidative skeletal muscles.GeroScience · 2026Article
- Pathological changes and therapeutic strategies for sarcopenia.EFORT open reviews · 2026Review
- Deuterated polyunsaturated fatty acids alleviate in vitro skeletal muscle dysfunction induced by oxidative stress.Free radical biology & medicine · 2026Article
- Structural and Metabolic Remodeling of Skeletal Muscle in Heart Failure with Reduced Ejection Fraction: A Review: Beyond the Failing Heart.International journal of molecular sciences · 2026Review
- Reactive oxygen species in health and disease.Molecular biomedicine · 2026Review
- Is Ferroptosis the Mechanistic Bridge Connecting Iron Dysregulation to Muscle Wasting and Functional Decline in Aging?Aging cell · 2026Review
- Current Progress in the Role of Ferroptosis in Skeletal Muscle Atrophy.Mediators of inflammation · 2026Review
- Deuterated Polyunsaturated Fatty Acids AlleviatebioRxiv : the preprint server for biology · 2025Article
- Role of Branched-Chain Amino Acids in Mitigating Osteosarcopenia: An Experimental Study Using Ovariectomised Mice Models.Journal of cachexia, sarcopenia and muscle · 2025Article
- N-acetylcarnosine attenuates age-associated declines in multi-organ systems to improve survival.bioRxiv : the preprint server for biology · 2025Article
- Molecular Framework of the Onset and Progression of Skeletal Muscle Aging.International journal of molecular sciences · 2025Review
- Iron supplementation alleviates pathologies in a mouse model of facioscapulohumeral muscular dystrophy.The Journal of clinical investigation · 2025Article
- A Reassessment of Sarcopenia from a Redox Perspective as a Basis for Preventive and Therapeutic Interventions.International journal of molecular sciences · 2025Review
- The role of adipose tissue in critical illness-induced skeletal muscle wasting-new considerations for treatment approaches.Journal of applied physiology (Bethesda, Md. : 1985) · 2025Review
- Association between morphological and mechanical properties of lower limb muscles and metabolic syndrome in type 2 diabetes.Diabetology & metabolic syndrome · 2025Article
- Taurine Attenuates Disuse Muscle Atrophy Through Modulation of the xCT-GSH-GPX4 and AMPK-ACC-ACSL4 Pathways.Antioxidants (Basel, Switzerland) · 2025Article
- Inhibition of mitochondrial fission protein Drp1 ameliorates skeletal myopathy in the D2-mdx model of Duchenne muscular dystrophy.American journal of physiology. Cell physiology · 2025Article
Corrections and comments
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Authors and funding
20 authors at 5 institutions in 3 countries.
Funding
Abstract
Reactive oxygen species (ROS) accumulation is a cardinal feature of skeletal muscle atrophy. ROS refers to a collection of radical molecules whose cellular signals are vast, and it is unclear which downstream consequences of ROS are responsible for the loss of muscle mass and strength. Here, we show that lipid hydroperoxides (LOOH) are increased with age and disuse, and the accumulation of LOOH by deletion of glutathione peroxidase 4 (GPx4) is sufficient to augment muscle atrophy. LOOH promoted atrophy in a lysosomal-dependent, proteasomal-independent manner. In young and old mice, genetic and pharmacological neutralization of LOOH or their secondary reactive lipid aldehydes robustly prevented muscle atrophy and weakness, indicating that LOOH-derived carbonyl stress mediates age- and disuse-induced muscle dysfunction. Our findings provide novel insights for the role of LOOH in sarcopenia including a therapeutic implication by pharmacological suppression.
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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.