ArticleThe Journal of physiology2010
The KATP channel is a molecular sensor of atrophy in skeletal muscle.
Article in The Journal of physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 47 citations in OpenAlex.
- A randomized pilot efficacy and safety trial of diazoxide choline controlled-release in patients with Prader-Willi syndrome.PloS one · 2019Trial
- Determinants and predictive performance of reduced muscle mass in elderly patients with type 2 diabetes: a retrospective study.Frontiers in endocrinology · 2026Article
- Article
- Effects of Hypoglycemic Agents on The Musculoskeletal System: A Comprehensive Review.Drug design, development and therapy · 2025Review
- Imaging of Sarcopenia in Type 2 Diabetes Mellitus.Clinical interventions in aging · 2024Review
- Diabetes Pharmacotherapy and its effects on the Skeletal Muscle Energy Metabolism.Mini reviews in medicinal chemistry · 2024Review
- Age Is Just a Number: Progress and Obstacles in the Discovery of New Candidate Drugs for Sarcopenia.Cells · 2023Review
- The Role of Ion Channels in Functional Gastrointestinal Disorders (FGID): Evidence of Channelopathies and Potential Avenues for Future Research and Therapeutic Targets.International journal of molecular sciences · 2023Review
- Pathogenesis and comprehensive treatment strategies of sarcopenia in elderly patients with type 2 diabetes mellitus.Frontiers in endocrinology · 2023Review
- Neuromuscular recovery from botulism involves multiple forms of compensatory plasticity.Frontiers in cellular neuroscience · 2023Article
- Effects of short-term unloading and active recovery on human motor unit properties, neuromuscular junction transmission and transcriptomic profile.The Journal of physiology · 2022Article
- Review
- Bisphosphonates Targeting Ion Channels and Musculoskeletal Effects.Frontiers in pharmacology · 2022Review
- Anti-diabetic drugs and sarcopenia: emerging links, mechanistic insights, and clinical implications.Journal of cachexia, sarcopenia and muscle · 2021Review
- Zoledronic Acid as a Novel Dual Blocker of KIR6.1/2-SUR2 Subunits of ATP-Sensitive KPharmaceutics · 2021Article
- Review
- Consequences of SUR2[A478V] Mutation in Skeletal Muscle of Murine Model of Cantu Syndrome.Cells · 2021Article
- Structure based analysis of KScientific reports · 2021Article
- The hydroxypropyl-β-cyclodextrin-minoxidil inclusion complex improves the cardiovascular and proliferative adverse effects of minoxidil in male rats: Implications in the treatment of alopecia.Pharmacology research & perspectives · 2020Article
- Pathophysiological Consequences of KATP Channel Overactivity and Pharmacological Response to Glibenclamide in Skeletal Muscle of a Murine Model of Cantù Syndrome.Frontiers in pharmacology · 2020Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The involvement of ATP-sensitive K(+) (K(ATP)) channels in the atrophy of slow-twitch (MHC-I) soleus (SOL) and fast-twitch (MHC-IIa) flexor digitorum brevis (FDB) muscles was investigated in vivo in 14-day-hindlimb-unloaded (14-HU) rats, an animal model of disuse, and in vitro in drug-induced muscle atrophy. Patch-clamp and gene expression experiments were performed in combination with measurements of fibre diameters used as an index of atrophy, and with MHC labelling in 14-HU rats and controls. A down-regulation of K(ATP) channel subunits Kir6.2, SUR1 and SUR2B with marked atrophy and incomplete phenotype transition were observed in SOL of 14-HU rats. The observed changes in K(ATP) currents were well correlated with changes in fibre diameters and SUR1 expression, as well as with MHC-IIa expression. Half of the SOL fibres of 14-HU rats had reduced diameter and K(ATP) currents and were labelled by MHC-I antibodies. Non-atrophic fibres were labelled by MHC-IIa (22%) antibodies and had enhanced K(ATP) currents, or were labelled by MHC-I (28%) antibodies but had normal current. FDB was not affected in 14-HU rats and this is related to the high expression/activity of Kir6.2/SUR1 subunits characterizing this muscle phenotype. The long-term incubation of the control muscles in vitro with the K(ATP) channel blocker glibenclamide (10(6)m) reduced the K(ATP) currents with atrophy and these effects were prevented by the K(ATP) channel opener diazoxide (10(4)m). The in vivo down-regulation of SUR1, and possibly of Kir6.2 and SUR2B, or their in vitro pharmacological blockade activates atrophic signalling in skeletal muscle. All these findings suggest a new role for the K(ATP) channel as a molecular sensor of atrophy.
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