Involvement of calpain in myonephropathic metabolic syndrome (MNMS)

Tsuji, Yoshifumi; Kambayashi, Jun-ichi; Shiba, Eiichi; Sakon, Masato; Kawasaki, Tomio; Mori, Takesada

doi:10.1016/s0950-821x(05)80969-7

Cited by 3 publications

(1 citation statement)

References 19 publications

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“…The mutations destroy the proteolytic activity of p94, and the lack of protease activity rather than an increase is the primary cause of the disease. Calpain might also play a significant role in myonephropathic metabolic syndrome (MNMS), a serious muscle reperfusion injury associated with acute renal failure, since administration of a calpain antagonist prevented MNMS (523). Dystrophin-deficient mouse muscles (mdx) contain higher calpain concentrations compared with controls (487).…”

Section: Calpainsmentioning

confidence: 99%

Calcium Ion in Skeletal Muscle: Its Crucial Role for Muscle Function, Plasticity, and Disease

Berchtold

Brinkmeier

Müntener

2000

Physiological Reviews

802

627

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Mammalian skeletal muscle shows an enormous variability in its functional features such as rate of force production, resistance to fatigue, and energy metabolism, with a wide spectrum from slow aerobic to fast anaerobic physiology. In addition, skeletal muscle exhibits high plasticity that is based on the potential of the muscle fibers to undergo changes of their cytoarchitecture and composition of specific muscle protein isoforms. Adaptive changes of the muscle fibers occur in response to a variety of stimuli such as, e.g., growth and differentition factors, hormones, nerve signals, or exercise. Additionally, the muscle fibers are arranged in compartments that often function as largely independent muscular subunits. All muscle fibers use Ca(2+) as their main regulatory and signaling molecule. Therefore, contractile properties of muscle fibers are dependent on the variable expression of proteins involved in Ca(2+) signaling and handling. Molecular diversity of the main proteins in the Ca(2+) signaling apparatus (the calcium cycle) largely determines the contraction and relaxation properties of a muscle fiber. The Ca(2+) signaling apparatus includes 1) the ryanodine receptor that is the sarcoplasmic reticulum Ca(2+) release channel, 2) the troponin protein complex that mediates the Ca(2+) effect to the myofibrillar structures leading to contraction, 3) the Ca(2+) pump responsible for Ca(2+) reuptake into the sarcoplasmic reticulum, and 4) calsequestrin, the Ca(2+) storage protein in the sarcoplasmic reticulum. In addition, a multitude of Ca(2+)-binding proteins is present in muscle tissue including parvalbumin, calmodulin, S100 proteins, annexins, sorcin, myosin light chains, beta-actinin, calcineurin, and calpain. These Ca(2+)-binding proteins may either exert an important role in Ca(2+)-triggered muscle contraction under certain conditions or modulate other muscle activities such as protein metabolism, differentiation, and growth. Recently, several Ca(2+) signaling and handling molecules have been shown to be altered in muscle diseases. Functional alterations of Ca(2+) handling seem to be responsible for the pathophysiological conditions seen in dystrophinopathies, Brody's disease, and malignant hyperthermia. These also underline the importance of the affected molecules for correct muscle performance.

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Section: Calpainsmentioning

confidence: 99%

Calcium Ion in Skeletal Muscle: Its Crucial Role for Muscle Function, Plasticity, and Disease

Berchtold

Brinkmeier

Müntener

2000

Physiological Reviews

802

627

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Myonephropathic Metabolic Syndrome After Bilateral Aortoiliac Bypass: A Pathogenic Role of Cholesterol Microemboli

Fujii¹,

Ueda²,

Oka³

et al. 1998

Vascular Surgery

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A 72-year-old man was admitted to our hospital for management of intermittent claudication. A preoperative angiogram showed right common iliac artery occlusion with wellmaintained peripheral flow via collaterals and 50% stenosis of the aortic bifurcation through the left common iliac artery. The authors performed bilateral aortoiliac artery bypass surgery. Immediately following the operation, the left lower limb was cyanotic and cold despite a good pulse in the left dorsalis pedis artery. He suffered from severe pain throughout his entire left calf and part of his thigh. Thrombolytic therapy combined with anticoagulation therapy was started in an attempt to reduce limb ischemia. However, swelling of the left calf increased, and clinical and metabolic manifestations consistent with myonephropathic metabolic syndrome (MNMS) developed. Serum creatine kinase and creatinine rose to 21,600 u/L and 2.8 mg/dl, respectively. His toe became necrotic and a transmetatarsal amputation was done. A skin biopsy taken from the edge of the amputation revealed cholesterol crystals within the capillaries. This report suggests that massive cholesterol microemboli are responsible for MNMS in this patient.

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An Elderly Patient with Leriche Syndrome Complicated by Congestive Heart Failure and Rhabdomyolysis.

Yabe

Matsumura²,

Furuno³

et al. 1996

Jpn. j. geriat

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Involvement of calpain in myonephropathic metabolic syndrome (MNMS)

Cited by 3 publications

References 19 publications

Calcium Ion in Skeletal Muscle: Its Crucial Role for Muscle Function, Plasticity, and Disease

Calcium Ion in Skeletal Muscle: Its Crucial Role for Muscle Function, Plasticity, and Disease

Myonephropathic Metabolic Syndrome After Bilateral Aortoiliac Bypass: A Pathogenic Role of Cholesterol Microemboli

An Elderly Patient with Leriche Syndrome Complicated by Congestive Heart Failure and Rhabdomyolysis.

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