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Myopathy caused by mammalian target of rapamycin complex 1 (mTORC1) inactivation is not reversed by restoring mitochondrial function

https://doi.org/10.1073/pnas.1111448109
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Inferred edges come from two machine sources: sweeps of open repository metadata (mostly SSRN and Zenodo), and a bulk OpenAlex citation snapshot. Every row below is labelled with the one it came from. Neither is a complete citation index — absence here is not evidence of absence.

2 of the 23 references listed on this page are in the Retraction Watch database as retracted (export 2026-10-21): 10.1016/j.cmet.2008.07.006 (notice 2016-12-13), 10.1073/pnas.0911570106 (notice 2016-12-19).

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What this work says

Outgoing claims: the papers this work cites, builds on, or argues with.

inferredcites →https://doi.org/10.1007/s00125-005-0068-4openalex-snapshot
The role of protein kinase B/Akt in insulin-induced inactivation of phosphorylase in rat hepatocytes
inferredcites →https://doi.org/10.1016/j.biocel.2005.04.018openalex-snapshot
Skeletal muscle hypertrophy and atrophy signaling pathways
inferredcites →https://doi.org/10.1016/j.cell.2006.01.016openalex-snapshot
TOR Signaling in Growth and Metabolism
inferredcites →https://doi.org/10.1016/j.cmet.2005.05.004openalex-snapshot
Metabolic control through the PGC-1 family of transcription coactivators
inferredcites →https://doi.org/10.1016/j.cmet.2008.07.006openalex-snapshot
RETRACTED: Activation of the PPAR/PGC-1α Pathway Prevents a Bioenergetic Deficit and Effectively Improves a Mitochondrial Myopathy Phenotype
inferredcites →https://doi.org/10.1016/j.cmet.2008.10.002openalex-snapshot
Skeletal Muscle-Specific Ablation of raptor, but Not of rictor, Causes Metabolic Changes and Results in Muscle Dystrophy
inferredcites →https://doi.org/10.1016/j.cmet.2009.10.008openalex-snapshot
Autophagy Is Required to Maintain Muscle Mass
inferredcites →https://doi.org/10.1016/s0092-8674(00)80611-xopenalex-snapshot
Mechanisms Controlling Mitochondrial Biogenesis and Respiration through the Thermogenic Coactivator PGC-1
inferredcites →https://doi.org/10.1038/nature00904openalex-snapshot
Transcriptional co-activator PGC-1α drives the formation of slow-twitch muscle fibres
inferredcites →https://doi.org/10.1038/nature02866openalex-snapshot
Absence of S6K1 protects against age- and diet-induced obesity while enhancing insulin sensitivity
inferredcites →https://doi.org/10.1038/nature05861openalex-snapshot
Akt/PKB regulates hepatic metabolism by directly inhibiting PGC-1α transcription coactivator
inferredcites →https://doi.org/10.1038/nature06322openalex-snapshot
mTOR controls mitochondrial oxidative function through a YY1–PGC-1α transcriptional complex
inferredcites →https://doi.org/10.1038/nm.2247openalex-snapshot
Autophagy is defective in collagen VI muscular dystrophies, and its reactivation rescues myofiber degeneration
inferredcites →https://doi.org/10.1073/pnas.0604893104openalex-snapshot
Lack of myostatin results in excessive muscle growth but impaired force generation
inferredcites →https://doi.org/10.1073/pnas.0607795103openalex-snapshot
PGC-1α protects skeletal muscle from atrophy by suppressing FoxO3 action and atrophy-specific gene transcription
inferredcites →https://doi.org/10.1073/pnas.0911570106openalex-snapshot
RETRACTED: Increased muscle PGC-1α expression protects from sarcopenia and metabolic disease during aging
inferredcites →https://doi.org/10.1074/jbc.m704817200openalex-snapshot
Skeletal Muscle Fiber-type Switching, Exercise Intolerance, and Myopathy in PGC-1α Muscle-specific Knock-out Animals
inferredcites →https://doi.org/10.1074/jbc.m707006200openalex-snapshot
A Role for the Transcriptional Coactivator PGC-1α in Muscle Refueling
inferredcites →https://doi.org/10.1083/jcb.200903131openalex-snapshot
Muscle inactivation of mTOR causes metabolic and dystrophin defects leading to severe myopathy
inferredcites →https://doi.org/10.1101/gad.1525107openalex-snapshot
PGC-1α regulates the neuromuscular junction program and ameliorates Duchenne muscular dystrophy
inferredcites →https://doi.org/10.1152/japplphysiol.00167.2002openalex-snapshot
Invited Review: Intracellular signaling in contracting skeletal muscle
inferredcites →https://doi.org/10.1186/1475-2840-4-14openalex-snapshot
Dual and pan-peroxisome proliferator-activated receptors (PPAR) co-agonism: the bezafibrate lessons
inferredcites →https://doi.org/10.1210/jc.2007-1701openalex-snapshot
Activation of Peroxisome Proliferator-Activated Receptor Pathway Stimulates the Mitochondrial Respiratory Chain and Can Correct Deficiencies in Patients’ Cells Lacking Its Components

What points at this work

Incoming claims: where this work appears in other papers’ reference lists and arguments.

inferred← citeshttps://doi.org/10.2139/ssrn.3919938openalex-extracted
Thyroid Hormone Regulates Glutamine Metabolism and Anaplerotic Fluxes by Inducing Mitochondrial Glutamine Aminotransferase GPT2
inferred← citeshttps://doi.org/10.1002/jcsm.12336openalex-snapshot
Lack of muscle mTOR kinase activity causes early onset myopathy and compromises whole‐body homeostasis
inferred← citeshttps://doi.org/10.1002/jcsm.12426openalex-snapshot
Chemotherapy‐induced cachexia dysregulates hypothalamic and systemic lipoamines and is attenuated by cannabigerol
inferred← citeshttps://doi.org/10.1002/jcsm.12505openalex-snapshot
mTORC1 signalling is not essential for the maintenance of muscle mass and function in adult sedentary mice
inferred← citeshttps://doi.org/10.1002/jcsm.12846openalex-snapshot
AKT controls protein synthesis and oxidative metabolism via combined mTORC1 and FOXO1 signalling to govern muscle physiology
inferred← citeshttps://doi.org/10.1007/s00018-025-05695-9openalex-snapshot
Muscle mTOR controls iron homeostasis and ferritinophagy via NRF2, HIFs and AKT/PKB signaling pathways
inferred← citeshttps://doi.org/10.1016/b978-0-12-810422-4.00003-8openalex-snapshot
Molecular Mechanisms of Postmeal Regulation of Muscle Anabolism
inferred← citeshttps://doi.org/10.1016/j.bcp.2014.06.014openalex-snapshot
Cyclosporine A enhances gluconeogenesis while sirolimus impairs insulin signaling in peripheral tissues after 3 weeks of treatment
inferred← citeshttps://doi.org/10.1016/j.ceb.2014.12.001openalex-snapshot
mTOR signaling in cellular and organismal energetics
inferred← citeshttps://doi.org/10.1016/j.celrep.2022.110409openalex-snapshot
Thyroid hormone regulates glutamine metabolism and anaplerotic fluxes by inducing mitochondrial glutamate aminotransferase GPT2
inferred← citeshttps://doi.org/10.1016/j.exer.2015.04.006openalex-snapshot
Loss of mTOR signaling affects cone function, cone structure and expression of cone specific proteins without affecting cone survival
inferred← citeshttps://doi.org/10.1016/j.gde.2012.12.005openalex-snapshot
mTOR in aging, metabolism, and cancer
inferred← citeshttps://doi.org/10.1016/j.neuroscience.2018.05.036openalex-snapshot
Constitutive PGC-1α Overexpression in Skeletal Muscle Does Not Improve Morphological Outcome in Mouse Models of Brain Irradiation or Cortical Stroke
inferred← citeshttps://doi.org/10.1016/j.yjmcc.2016.04.011openalex-snapshot
mTOR inactivation in myocardium from infant mice rapidly leads to dilated cardiomyopathy due to translation defects and p53/JNK-mediated apoptosis
inferred← citeshttps://doi.org/10.1038/s41392-025-02493-4openalex-snapshot
mTOR signaling networks: mechanistic insights and translational frontiers in disease therapeutics
inferred← citeshttps://doi.org/10.1038/s41574-023-00934-0openalex-snapshot
mTORC1 in energy expenditure: consequences for obesity
inferred← citeshttps://doi.org/10.1038/s41598-017-14063-yopenalex-snapshot
A Skeletal Muscle Model of Infantile-onset Pompe Disease with Patient-specific iPS Cells
inferred← citeshttps://doi.org/10.1038/srep37223openalex-snapshot
mTORC1 is Required for Brown Adipose Tissue Recruitment and Metabolic Adaptation to Cold
inferred← citeshttps://doi.org/10.1039/c9fo02489aopenalex-snapshot
A pilot study on the effects of DHA/EPA-enriched phospholipids on aerobic and anaerobic exercises in mice
inferred← citeshttps://doi.org/10.1073/pnas.1312039110openalex-snapshot
The transcriptional coactivator PGC-1α is dispensable for chronic overload-induced skeletal muscle hypertrophy and metabolic remodeling
inferred← citeshttps://doi.org/10.1080/13880209.2020.1756349openalex-snapshot
Berberine attenuates fructose-induced insulin resistance by stimulating the hepatic LKB1/AMPK/PGC1α pathway in mice
inferred← citeshttps://doi.org/10.1101/738294openalex-snapshot
mTORC1 signaling is not essential for the maintenance of muscle mass and function in adult sedentary mice
inferred← citeshttps://doi.org/10.1124/jpet.114.214700openalex-snapshot
Agonism of the 5-Hydroxytryptamine 1F Receptor Promotes Mitochondrial Biogenesis and Recovery from Acute Kidney Injury
inferred← citeshttps://doi.org/10.1139/apnm-2012-0405openalex-snapshot
Mammalian target of rapamycin pathway is up-regulated by both acute endurance exercise and chronic muscle contraction in rat skeletal muscle
inferred← citeshttps://doi.org/10.1139/cjpp-2018-0501openalex-snapshot
Restoration of skeletal muscle homeostasis by hydrogen sulfide during hyperhomocysteinemia-mediated oxidative/ER stress condition
inferred← citeshttps://doi.org/10.1146/annurev-nutr-071714-034355openalex-snapshot
The Roles of mTOR Complexes in Lipid Metabolism
inferred← citeshttps://doi.org/10.1152/ajpcell.00156.2012openalex-snapshot
Contractile activity-induced mitochondrial biogenesis and mTORC1
inferred← citeshttps://doi.org/10.1152/ajpheart.00877.2012openalex-snapshot
Regulation of fatty acid metabolism by mTOR in adult murine hearts occurs independently of changes in PGC-1α
inferred← citeshttps://doi.org/10.1152/ajpregu.00241.2022openalex-snapshot
Adult skeletal muscle peroxisome proliferator-activated receptor γ -related coactivator 1 is involved in maintaining mitochondrial content
inferred← citeshttps://doi.org/10.1186/2044-5040-2-14openalex-snapshot
IL-6 regulation on skeletal muscle mitochondrial remodeling during cancer cachexia in the Apc Min/+ mouse
inferred← citeshttps://doi.org/10.1186/2044-5040-3-6openalex-snapshot
Differential response of skeletal muscles to mTORC1 signaling during atrophy and hypertrophy
inferred← citeshttps://doi.org/10.1186/s13395-016-0084-8openalex-snapshot
Alterations to mTORC1 signaling in the skeletal muscle differentially affect whole-body metabolism
inferred← citeshttps://doi.org/10.1242/jcs.125773openalex-snapshot
Regulation of mTORC1 and its impact on gene expression at a glance
inferred← citeshttps://doi.org/10.1371/journal.pcbi.1003728openalex-snapshot
Dynamic Modelling of Pathways to Cellular Senescence Reveals Strategies for Targeted Interventions
inferred← citeshttps://doi.org/10.15252/embj.201592862openalex-snapshot
Mitochondria are required for pro‐ageing features of the senescent phenotype
inferred← citeshttps://doi.org/10.1681/asn.2018010050openalex-snapshot
Phosphorylation of Acetyl-CoA Carboxylase by AMPK Reduces Renal Fibrosis and Is Essential for the Anti-Fibrotic Effect of Metformin
inferred← citeshttps://doi.org/10.18297/etd/3114openalex-snapshot
Effects of hydrogen sulfide in hyperhomocysteinemia-mediated skeletal muscle myopathy.
inferred← citeshttps://doi.org/10.18632/aging.100576openalex-snapshot
Rapamycin doses sufficient to extend lifespan do not compromise muscle mitochondrial content or endurance
inferred← citeshttps://doi.org/10.26508/lsa.202402991openalex-snapshot
Metabolic dysregulation contributes to the development of dysferlinopathy
inferred← citeshttps://doi.org/10.3390/cells1030325openalex-snapshot
Autophagy in Skeletal Muscle Homeostasis and in Muscular Dystrophies
inferred← citeshttps://doi.org/10.3390/cells8040289openalex-snapshot
Mitochondrial Genetic Disorders: Cell Signaling and Pharmacological Therapies
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