Rapamycin Reverses Elevated mTORC1 Signaling in Lamin A/C–Deficient Mice, Rescues Cardiac and Skeletal Muscle Function, and Extends Survival
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Rapamycin treatment of a mouse model for a human laminopathy improves cardiac and muscle function, suggesting a therapy for human patients.
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Defective autophagy plays a role in congenital muscular dystrophies caused by defects in collagen VI production, laminin A/C, or dystrophin.
“Defective autophagy plays a role in congenital muscular dystrophies caused by defects in collagen VI production [243], laminin A/C [244] or dystrophin [245].”
From The connection between the dynamic remodeling of the mitochondrial network and the regulation of muscle mass (2021) · cites this paper as [244]
Autophagy flux reactivation by dietary or pharmacological tools, like rapamycin, cyclosporine A, or AICAR, rescues the dystrophic phenotype by clearing the abnormal mitochondria.
“Importantly, autophagy flux reactivation by dietary or pharmacological tools, like rapamycin, cyclosporine A, or AICAR, rescues the dystrophic phenotype by clearing the abnormal mitochondria [243–246].”
From The connection between the dynamic remodeling of the mitochondrial network and the regulation of muscle mass (2021) · cites this paper as [244]
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References 66 · Cited by 349
Research works printed but not linked: 1
- [46]Grumati P Coletto L Sabatelli P Cescon M Angelin A Bertaggia E Blaauw B Urciuolo A Tiepolo T Merlini L Maraldi NM Bernardi P Sandri M Bonaldo P Autophagy is defective in collagen VI muscular dystrophies, and its reactivation rescues myofiber degeneration. Nat. Med 2010 16 1313 1320 21037586
- Authors
- Ramos, F. J., Chen, S. C., Garelick, M. G., Dai, D.-F., Liao, C.-Y., Schreiber, K. H., MacKay, V. L., An, E. H., Strong, R., Ladiges, W. C., Rabinovitch, P. S., Kaeberlein, M., & Kennedy, B. K.
- Affiliations
- University of Washington (US)
- Buck Institute for Research on Aging (US)
- The University of Texas at San Antonio Health Science Center (US)
- Corresponding author
- Kaeberlein, Matt
- Kennedy, Brian K.
- ORCID
- Venue
- Science Translational Medicine
- Published
- 2012-07-25
- Volume
- 4
- Issue
- 144
- Pages
- 144ra103-144ra103
- ISSN
- 1946-6234 (ISSN-L)
- 1946-6242
- PMC
- PMC3613228
- OpenAlex
- W2126297812
- Cited by
- 349
- References
- 66
- Citations by year
- 2026: 5 · 2025: 17 · 2024: 21 · 2023: 26 · 2022: 13 · 2021: 29 · 2020: 26 · 2019: 21 · 2018: 35 · 2017: 25 · 2016: 38 · 2015: 21 · 2014: 39 · 2013: 23 · 2012: 10
- FWCI
- 11.94
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- Science Translational Medicine (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute on Aging (T32AG000057, R01AG033373, P01AG001751, R01AG024287, R01AG038550, U01AG022307, P30AG013280)
- National Heart, Lung, and Blood Institute (T32HL007312)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nuclear Structure and Function
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiomyopathy and Myosin Studies
- Keywords
- rapamycin, mTORC1 signaling, lamin A/C, laminopathies, dilated cardiomyopathy, skeletal muscle dystrophy, autophagy, mTORC1 inhibitors, cardiac function, survival
- MeSH terms
- Mechanistic Target of Rapamycin Complex 1, Animals, Desmin, Female, Heart, Male, Myocardium, Proteins, Signal Transduction, Muscle, Skeletal, Sirolimus, Lamin Type A, Multiprotein Complexes, Mice, TOR Serine-Threonine Kinases
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