ArticleFree radical biology & medicine2018
Mitochondrial protein S-nitrosation protects against ischemia reperfusion-induced denervation at neuromuscular junction in skeletal muscle.
Article in Free radical biology & medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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.
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
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.
- Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)Autophagy · 2021Guideline
- S-nitrosoglutathione preserves vasodilation and attenuates myocardial ischemia-reperfusion injury.Scientific reports · 2026Article
- CORP: In vivo muscle strength-perspectives on the design and interpretation of preclinical animal studies.American journal of physiology. Regulatory, integrative and comparative physiology · 2025Review
- Targeted Redox Regulation α-Ketoglutarate Dehydrogenase Complex for the Treatment of Human Diseases.Cells · 2025Review
- Neuromuscular Dysfunction Precedes Cognitive Impairment in a Mouse Model of Alzheimer's Disease.Function (Oxford, England) · 2024Article
- Unraveling the causes of sarcopenia: Roles of neuromuscular junction impairment and mitochondrial dysfunction.Physiological reports · 2024Review
- ND3 Cys39 in complex I is exposed during mitochondrial respiration.Cell chemical biology · 2022Article
- Effect of chronic intermittent hypoxia (CIH) on neuromuscular junctions and mitochondria in slow- and fast-twitch skeletal muscles of mice-the role of iNOS.Skeletal muscle · 2022Article
- Mitochondria-localized AMPK responds to local energetics and contributes to exercise and energetic stress-induced mitophagy.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Skeletal Muscle Mitochondrial Dysfunction and Oxidative Stress in Peripheral Arterial Disease: A Unifying Mechanism and Therapeutic Target.Antioxidants (Basel, Switzerland) · 2020Review
- Long-term voluntary running prevents the onset of symptomatic Friedreich's ataxia in mice.Scientific reports · 2020Article
- Precision remodeling: how exercise improves mitochondrial quality in myofibers.Current opinion in physiology · 2019Article
- Critical Limb Ischemia Induces Remodeling of Skeletal Muscle Motor Unit, Myonuclear-, and Mitochondrial-Domains.Scientific reports · 2019Article
- Voluntary running protects against neuromuscular dysfunction following hindlimb ischemia-reperfusion in mice.Journal of applied physiology (Bethesda, Md. : 1985) · 2019Article
- Mitochondria as a therapeutic target for common pathologies.Nature reviews. Drug discovery · 2018Review
- Mitochondrial ROS cause motor deficits induced by synaptic inactivity: Implications for synapse pruning.Redox biology · 2018Article
- When motor unit expansion in ageing muscle fails, atrophy ensues.The Journal of physiology · 2018Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
Deterioration of neuromuscular junction (NMJ) integrity and function is causal to muscle atrophy and frailty, ultimately hindering quality of life and increasing the risk of death. In particular, NMJ is vulnerable to ischemia reperfusion (IR) injury when blood flow is restricted followed by restoration. However, little is known about the underlying mechanism(s) and hence the lack of effective interventions. New evidence suggests that mitochondrial oxidative stress plays a causal role in IR injury, which can be precluded by enhancing mitochondrial protein S-nitrosation (SNO). To elucidate the role of IR and mitochondrial protein SNO in skeletal muscle, we utilized a clinically relevant model and showed that IR resulted in significant muscle and motor nerve injuries with evidence of elevated muscle creatine kinase in the serum, denervation at NMJ, myofiber degeneration and regeneration, as well as muscle atrophy. Interestingly, we observed that neuromuscular transmission improved prior to muscle recovery, suggesting the importance of the motor nerve in muscle functional recovery. Injection of a mitochondria-targeted S-nitrosation enhancing agent, MitoSNO, into ischemic muscle prior to reperfusion reduced mitochondrial oxidative stress in the motor nerve and NMJ, attenuated denervation at NMJ, and resulted in accelerated functional recovery of the muscle. These findings demonstrate that enhancing mitochondrial protein SNO protects against IR-induced denervation at NMJ in skeletal muscle and accelerates functional regeneration. This could be an efficacious intervention for protecting neuromuscular injury under the condition of IR and other related pathological conditions.
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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.