Lanner Lab - Molecular muscle physiology and pathophysiology
We study molecular mechanisms underlying muscle remodeling and contractile dysfunction. We are also involved in forming novel therapeutic interventions to treat skeletal muscle weakness.
Our body consists to ~50% of skeletal muscles, which are crucial for our ability to breathe and move. Skeletal muscle is also a primary site for glucose uptake and a reservoir of amino acids stored as protein. Muscle dysfunction, comprising muscle weakness and altered metabolism, is a common comorbidity in many non-communicable diseases, such as type 2 diabetes, peripheral artery disease, rheumatoid arthritis, and cancer, as well as normal ageing. Muscle dysfunction can reduce both the ability to work and the quality of life for afflicted patients and is considered to accelerate mortality.
Our lab focuses on deciphering the molecular mechanisms that contributes to disease-induced muscle dysfunction and identifying novel therapeutic interventions to counteract muscle weakness. Altered Ca2+ handling, free radical signaling and mitochondrial function are key factors in the intramuscular interplay that may contribute to impaired muscle function and hence central components in our research.
In the lab, we currently have projects related to muscle dysfunction associated with rheumatoid arthritis (RA), obesity and type 2 diabetes (T2D) and breast cancer.
We apply a multidisciplinary translational approach involving in vivo and in vitro analysis in mice and humans, including force measurements, live imaging of Ca2+ and free radicals, metabolic profiles, mass spectrometry, and biochemical and molecular assays.
The Lanner lab research team currently consist of:
Exercise reduces intramuscular stress and counteracts muscle weakness in mice with breast cancer
Mader T, Chaillou T, Santos Alves E, Jude B, Cheng A J, Kenne E, Mijwel, Kurzejamska E, Vincent C T, Rundqvist H, Lanner J T.
J Cachexia Sarcopenia Muscle. 2022 Feb 15
Mitochondrial NDUFA4L2 is a novel regulator of skeletal muscle mass and force
Liu Z, Chaillou T, Santos Alves E, Mader T, Jude B, Ferreira D M S, Hynynen H, Cheng A J, Jonsson W O, Pironti G, Andersson D C, Kenne E, Ruas J L, Tavi P, Lanner J T
FASEB J. 2021 Dec
Skeletal muscle redox signaling in rheumatoid arthritis.
Steinz MM, Santos-Alves E, Lanner JT
Clin Sci (Lond) 2020 Nov;134(21):2835-2850
Intramuscular mechanisms of overtraining.
Cheng AJ, Jude B, Lanner JT
Redox Biol 2020 08;35():101480
Skeletal muscle PGC-1α1 reroutes kynurenine metabolism to increase energy efficiency and fatigue-resistance.
Agudelo LZ, Ferreira DMS, Dadvar S, Cervenka I, Ketscher L, Izadi M, Zhengye L, Furrer R, Handschin C, Venckunas T, Brazaitis M, Kamandulis S, Lanner JT, Ruas JL
Nat Commun 2019 06;10(1):2767
Oxidative hotspots on actin promote skeletal muscle weakness in rheumatoid arthritis.
Steinz MM, Persson M, Aresh B, Olsson K, Cheng AJ, Ahlstrand E, et al
JCI Insight 2019 Mar;5():
SR Ca2+ leak in skeletal muscle fibers acts as an intracellular signal to increase fatigue resistance.
Ivarsson N, Mattsson CM, Cheng AJ, Bruton JD, Ekblom B, Lanner JT, Westerblad H
J Gen Physiol 2019 04;151(4):567-577
Reactive oxygen/nitrogen species and contractile function in skeletal muscle during fatigue and recovery.
Cheng AJ, Yamada T, Rassier DE, Andersson DC, Westerblad H, Lanner JT
J. Physiol. (Lond.) 2016 09;594(18):5149-60
Muscle dysfunction associated with adjuvant-induced arthritis is prevented by antioxidant treatment.
Yamada T, Abe M, Lee J, Tatebayashi D, Himori K, Kanzaki K, et al
Skelet Muscle 2015 ;5():20
Nitrosative modifications of the Ca2+ release complex and actin underlie arthritis-induced muscle weakness.
Yamada T, Fedotovskaya O, Cheng AJ, Cornachione AS, Minozzo FC, Aulin C, et al
Ann. Rheum. Dis. 2015 Oct;74(10):1907-14
- Foreum, Fondation for Research in Rheumatology
- Olle Engkvist Foundation (web page in Swedish)
- Swedish Research Council
- Diabetesfonden (web page in Swedish)
- SRP Diabetes
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