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- 1. 心筋における興奮収縮連関 excitation contraction coupling in myocardium
- 2. 拡張能障害の細胞学的機序 cellular mechanisms of diastolic dysfunction
- 3. 低カルシウム血症の臨床症状 clinical manifestations of hypocalcemia
- 4. 筋強直性ジストロフィー：病因、臨床的特徴、および診断 myotonic dystrophy etiology clinical features and diagnosis
- 5. 低カリウム性周期性四肢麻痺 hypokalemic periodic paralysis
- Regulatory role of regucalcin in heart calcium signaling: Insight into cardiac failure (Review).
- Yamaguchi M.Author information Department of Hematology and Medical Oncology, Emory University School of Medicine, Atlanta, GA 30322, USA.AbstractRegucalcin was first identified in 1978 as a regulatory protein of Ca2+ signaling in liver cells. Regucalcin was shown to play a multifunctional role in cell regulation, such as maintainance of intracellular Ca2+ homeostasis and suppression of signal transduction, protein synthesis, nuclear function, cell proliferation and apoptosis in various types of cells and tissues. Cardiac excitation-contraction coupling is based on the regulation of intracellular Ca2+ concentration by the Ca2+ pump in the sarcoplasmic reticulum of heart muscle cells. Regucalcin, which is expressed in the heart, was found to increase rat heart sarcoplasmic reticulum Ca2+-ATPase activity and ATP-dependent Ca2+ uptake and mitochondrial Ca2+-ATPase activity. Regucalcin was also shown to suppress Ca2+-dependent protein tyrosine phosphatase, Ca2+/calmodulin-dependent protein phosphatase (calcineurin) and nitric oxide (NO) synthase activity in the heart cytoplasm. Moreover, regucalcin was found to activate superoxide dismutase (SOD), which plays a significant role in the prevention of cell death and apoptosis in the heart. Regucalcin may be a key molecule in heart muscle cell regulation through Ca2+ signaling. Regucalcin may also play a pathophysiological role in heart failure. The aim of this study was to review the recent findings regarding the role of regucalcin in Ca2+ signaling in the heart.
- Biomedical reports.Biomed Rep.2014 May;2(3):303-308. Epub 2014 Mar 5.
- Regucalcin was first identified in 1978 as a regulatory protein of Ca2+ signaling in liver cells. Regucalcin was shown to play a multifunctional role in cell regulation, such as maintainance of intracellular Ca2+ homeostasis and suppression of signal transduction, protein synthesis, nuclear function
- PMID 24748964
- Computational analysis of Ca2+ dynamics in isolated cardiac mitochondria predicts two distinct modes of Ca2+ uptake.
- Tewari SG1, Camara AK, Stowe DF, Dash RK.Author information 1Biotechnology and Bioengineering Center, Medical College of Wisconsin, 8701 Watertown Plank Road, Milwaukee, WI 53226-6509, USA. email@example.com.AbstractCardiac mitochondria can act as a significant Ca2+ sink and shape cytosolic Ca2+ signals affecting various cellular processes, such as energy metabolism and excitation-contraction coupling. However, different mitochondrial Ca2+ uptake mechanisms are still not well understood. In this study, we analysed recently published Ca2+ uptake experiments performed on isolated guinea pig cardiac mitochondria using a computer model of mitochondrial bioenergetics and cation handling. The model analyses of the data suggest that the majority of mitochondrial Ca2+ uptake, at physiological levels of cytosolic Ca2+ and Mg2+, occurs through a fast Ca2+ uptake pathway, which is neither the Ca2+ uniporter nor the rapid mode of Ca2+ uptake. This fast Ca2+ uptake component was explained by including a biophysical model of the ryanodine receptor (RyR) in the computer model. However, the Mg2+-dependent enhancement of the RyR adaptation was not evident in this RyR-type channel, in contrast to that of cardiac sarcoplasmic reticulum RyR. The extended computer model is corroborated by simulating an independent experimental dataset, featuring mitochondrial Ca2+ uptake, egress and sequestration. The model analyses of the two datasets validate the existence of two classes of Ca2+ buffers that comprise the mitochondrial Ca2+ sequestration system. The modelling study further indicates that the Ca2+ buffers respond differentially depending on the source of Ca2+ uptake. In particular, it suggests that the Class 1 Ca2+ buffering capacity is auto-regulated by the rate at which Ca2+ is taken up by mitochondria.
- The Journal of physiology.J Physiol.2014 May 1;592(Pt 9):1917-1930. Epub 2014 Mar 3.
- Cardiac mitochondria can act as a significant Ca2+ sink and shape cytosolic Ca2+ signals affecting various cellular processes, such as energy metabolism and excitation-contraction coupling. However, different mitochondrial Ca2+ uptake mechanisms are still not well understood. In this study, we analy
- PMID 24591571
- β(2)-Adrenergic and M(2)-muscarinic receptors decrease basal t-tubular L-type Ca2+ channel activity and suppress ventricular contractility in heart failure
- Kashihara Toshihide,Hirose Masamichi,Shimojo Hisashi,Nakada Tsutomu,Gomi Simmon,Hongo Minoru,Yamada Mitsuhiko
- EUROPEAN JOURNAL OF PHARMACOLOGY 724, 122-131, 2014-02-05
- … L-Lype Ca2+ channels (LTCC) play a crucial role in cardiac excitation-contraction coupling. …
- NAID 120005440173
- 幼少期の心機能を制御する新しいCa2+ 調節タンパク質の発見とその分子機構
- 中村（西谷） 友重,若林 繁夫
- 日本小児循環器学会雑誌 30(3), 224-231, 2014
- 心臓の収縮や心肥大・心不全の発症を調節するものとして，細胞内カルシウム（Ca2+）の増減が重要なカギとなっている．しかし，胎児期や幼少期などの未成熟期の心臓では，細胞内Ca2+貯蔵装置である筋小胞体（SR）の構造が成体と比べはるかに未発達であることから，どのようにCa2+による収縮調節を行っているのか不明な点が多かった．今回，特に未成熟期の心臓に高発現するCa2+結合タンパク質（Neuronal …
- NAID 130004879017
- Excitation Contraction Coupling Like most excitable cells, muscle fibers respond to the excitation signal with a rapid depolarization which is coupled with its physiological response: contraction. Cellular Resting Potential If we ...
- Although hormonal and biochemical changes play a vital role in regulating and developing conditions leading to labor, the speed and coordination of a process called excitation-contraction coupling in uterine muscle tissue indicate that ...