Molecular muscle physiology and pathophysiology

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We study molecular mechanisms behind muscle remodeling and contractile dysfunction. We are also involved in developing novel therapeutic interventions to treat skeletal muscle weakness. 

The lab has three overall goals:

I. Elucidate the role of Ca2+ and free radicals in driving skeletal muscle remodeling.
II. Identify and understand the mechanisms behind disease-induced muscle weakness.
III. Develop novel therapeutic interventions to treat skeletal muscle weakness.

We use a wide variety of methods to study these processes, ranging from single proteins via intact muscles to in vivo experiments and translational in humans.

Research in our laboratory

Calcium (Ca2+) is essential for muscle contraction and plays a central role in our research. In fact, every step you take is dependent on Ca2+ release from the major intracellular Ca2+ release channel, the ryanodine receptor (RyR). With this in mind it is easy to envisage that disturbed Ca2+ handling results in both skeletal muscle dysfunction.

Severe illnesses, such as rheumatoid arthritis, diabetes, renal failure and cancer, are commonly associated with secondary muscle complications, such as weakness. These muscle complications may even be the dominating symptom by reducing the quality of life for afflicted patients, since ordinary daily activities require extensive effort, and in the worst case cause premature mortality. Reduced muscle strength has traditionally been associated with decreased muscle mass. However, muscle weakness is not only a result of atrophic muscles, intracellular (intrinsic) muscle dysfunction also strongly contributes to impaired force production and muscle weakness. In our lab, we aim to identify and understand the molecular mechanisms behind muscle remodeling and contractile dysfunction. We are also involved in developing novel therapeutic interventions to counteract muscle weakness to improve muscle function.

Group members

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Financial support

Selected publications

Muscle Weakness in Rheumatoid Arthritis: The Role of Ca and Free Radical Signaling.
Yamada T, Steinz M, Kenne E, Lanner J
EBioMedicine 2017 Sep;23():12-19

Neuromuscular electrical stimulation prevents skeletal muscle dysfunction in adjuvant-induced arthritis rat.
Himori K, Tatebayashi D, Kanzaki K, Wada M, Westerblad H, Lanner J, et al
PLoS ONE 2017 ;12(6):e0179925

Docetaxel does not impair skeletal muscle force production in a murine model of cancer chemotherapy.
Chaillou T, McPeek A, Lanner J
Physiol Rep 2017 Jun;5(11):

Superoxide dismutase/catalase mimetic EUK-134 prevents diaphragm muscle weakness in monocrotalin-induced pulmonary hypertension.
Himori K, Abe M, Tatebayashi D, Lee J, Westerblad H, Lanner J, et al
PLoS ONE 2017 ;12(2):e0169146

Regulation of myogenesis and skeletal muscle regeneration: effects of oxygen levels on satellite cell activity.
Chaillou T, Lanner J
FASEB J. 2016 12;30(12):3929-3941

Reactive oxygen/nitrogen species and contractile function in skeletal muscle during fatigue and recovery.
Cheng A, Yamada T, Rassier D, Andersson D, Westerblad H, Lanner J
J. Physiol. (Lond.) 2016 09;594(18):5149-60

Ryanodine receptor fragmentation and sarcoplasmic reticulum Ca2+ leak after one session of high-intensity interval exercise.
Place N, Ivarsson N, Venckunas T, Neyroud D, Brazaitis M, Cheng A, et al
Proc. Natl. Acad. Sci. U.S.A. 2015 Dec;112(50):15492-7

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 A, Cornachione A, Minozzo F, Aulin C, et al
Ann. Rheum. Dis. 2015 Oct;74(10):1907-14

AICAR prevents heat-induced sudden death in RyR1 mutant mice independent of AMPK activation.
Lanner J, Georgiou D, Dagnino-Acosta A, Ainbinder A, Cheng Q, Joshi A, et al
Nat. Med. 2012 Jan;18(2):244-51

Ryanodine receptor physiology and its role in disease.
Lanner J
Adv. Exp. Med. Biol. 2012 ;740():217-34

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Physiology