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myofibrillar hypertrophy

Jakob Agergaard, Jacob Bulow, Jacob K Jensen, Søren Reitelseder, Micah J Drummond, Peter Schjerling, Thomas Scheike, Anja Serena, Lars Holm
INTRODUCTION: The present study investigated whether well-tolerated light-load resistance exercise (LL-RE) affects skeletal muscle fractional synthetic rate (FSR) and anabolic intracellular signaling as a way to counteract age-related loss of muscle mass. METHODS: Untrained healthy men (age: +65 yrs) were subjected to 13 hours supine rest. After 21/2 hours of rest, unilateral LL-RE was conducted consisting of leg extensions (10 sets, 36 repetitions) at 16% 1RM. Subsequently, the subjects were randomized to oral intake of PULSE (4g whey protein/hour; N=10), BOLUS (28g whey protein at 0 hours and 12g whey protein at 7 hours post-exercise; N=10) or placebo (4g maltodextrin/hour; N=10)...
October 25, 2016: American Journal of Physiology. Endocrinology and Metabolism
Amy E Vincent, John P Grady, Mariana C Rocha, Charlotte L Alston, Karolina A Rygiel, Rita Barresi, Robert W Taylor, Doug M Turnbull
Myofibrillar myopathies (MFM) are characterised by focal myofibrillar destruction and accumulation of myofibrillar elements as protein aggregates. They are caused by mutations in the DES, MYOT, CRYAB, FLNC, BAG3, DNAJB6 and ZASP genes as well as other as yet unidentified genes. Previous studies have reported changes in mitochondrial morphology and cellular positioning, as well as clonally-expanded, large-scale mitochondrial DNA (mtDNA) deletions and focal respiratory chain deficiency in muscle of MFM patients...
October 2016: Neuromuscular Disorders: NMD
Shiguo Li, Chao Liu, Lei Gu, Lina Wang, Yongliang Shang, Qiong Liu, Junyi Wan, Jian Shi, Fang Wang, Zhiliang Xu, Guangju Ji, Wei Li
Cardiovascular disease (CVD) is the leading cause of the death worldwide. An increasing number of studies have found that autophagy is involved in the progression or prevention of CVD. However, the precise mechanism of autophagy in CVD, especially the myocardial ischaemia-reperfusion injury (MI/R injury), is unclear and controversial. Here, we show that the cardiomyocyte-specific disruption of autophagy by conditional knockout of Atg7 leads to severe contractile dysfunction, myofibrillar disarray and vacuolar cardiomyocytes...
August 2016: Open Biology
E Leibing, T Meyer
Owing to its acute psychotropic effects, ethanol is the most frequently consumed toxic agent worldwide. However, excessive alcohol intake results in an array of health, social, and economic consequences, which are related to its property as an addictive substance. It has been well established that exposure to high levels of alcohol for a long period leads to the onset and progression of nonischemic cardiomyopathy through direct toxic mechanisms of ethanol and its metabolite, acetaldehyde. Excessive alcohol ingestion causes myocardial damage including disruptions of the myofibrillar architecture and is associated with reduced myocardial contractility and decreased ejection volumes...
September 2016: Herz
Felipe Damas, Stuart M Phillips, Cleiton A Libardi, Felipe C Vechin, Manoel E Lixandrão, Paulo R Jannig, Luiz A R Costa, Aline V Bacurau, Tim Snijders, Gianni Parise, Valmor Tricoli, Hamilton Roschel, Carlos Ugrinowitsch
KEY POINTS: Skeletal muscle hypertrophy is one of the main outcomes from resistance training (RT), but how it is modulated throughout training is still unknown. We show that changes in myofibrillar protein synthesis (MyoPS) after an initial resistance exercise (RE) bout in the first week of RT (T1) were greater than those seen post-RE at the third (T2) and tenth week (T3) of RT, with values being similar at T2 and T3. Muscle damage (Z-band streaming) was the highest during post-RE recovery at T1, lower at T2 and minimal at T3...
September 15, 2016: Journal of Physiology
Hidetoshi Suzuki, Yasufumi Katanasaka, Yoichi Sunagawa, Yusuke Miyazaki, Masafumi Funamoto, Hiromichi Wada, Koji Hasegawa, Tatsuya Morimoto
The zinc finger protein GATA4 is a transcription factor involved in cardiomyocyte hypertrophy. It forms a functional complex with the intrinsic histone acetyltransferase (HAT) p300. The HAT activity of p300 is required for the acetylation and transcriptional activity of GATA4, as well as for cardiomyocyte hypertrophy and the development of heart failure. In the present study, we have identified Receptor for Activated Protein Kinase C1 (RACK1) as a novel GATA4-binding protein using tandem affinity purification and mass spectrometry analyses...
September 2016: Biochimica et Biophysica Acta
Teet Seene, Priit Kaasik
Muscle weakness in corticosteroid myopathy is mainly the result of the destruction and atrophy of the myofibrillar compartment of fast-twitch muscle fibers. Decrease of titin and myosin, and the ratio of nebulin and MyHC in myopathic muscle, shows that these changes of contractile and elastic proteins are the result of increased catabolism of the abovementioned proteins in skeletal muscle. Slow regeneration of skeletal muscle is in good correlation with a decreased number of satellite cells under the basal lamina of muscle fibers...
2016: Metabolites
Viola Kooij, Meera C Viswanathan, Dong I Lee, Peter P Rainer, William Schmidt, William A Kronert, Sian E Harding, David A Kass, Sanford I Bernstein, Jennifer E Van Eyk, Anthony Cammarato
AIMS: Heart failure is often preceded by cardiac hypertrophy, which is characterized by increased cell size, altered protein abundance, and actin cytoskeletal reorganization. Profilin is a well-conserved, ubiquitously expressed, multifunctional actin-binding protein, and its role in cardiomyocytes is largely unknown. Given its involvement in vascular hypertrophy, we aimed to test the hypothesis that profilin-1 is a key mediator of cardiomyocyte-specific hypertrophic remodelling. METHODS AND RESULTS: Profilin-1 was elevated in multiple mouse models of hypertrophy, and a cardiomyocyte-specific increase of profilin in Drosophila resulted in significantly larger heart tube dimensions...
May 15, 2016: Cardiovascular Research
Helmut Kern, Ugo Carraro
We will here discuss the following points related to Home-based Functional Electrical Stimulation (h-b FES) as treatment for patients with permanently denervated muscles in their legs: 1. Upper (UMN) and lower motor neuron (LMN) damage to the lower spinal cord; 2. Muscle atrophy/hypertrophy versus processes of degeneration, regeneration, and recovery; 3. Recovery of twitch- and tetanic-contractility by h-b FES; 4. Clinical effects of h-b FES using the protocol of the "Vienna School"; 5. Limitations and perspectives...
March 31, 2014: European Journal of Translational Myology
Huaxiao Yang, Lucas P Schmidt, Zhonghai Wang, Xiaoqi Yang, Yonghong Shao, Thomas K Borg, Roger Markwald, Raymond Runyan, Bruce Z Gao
An increase in mechanical load in the heart causes cardiac hypertrophy, either physiologically (heart development, exercise and pregnancy) or pathologically (high blood pressure and heart-valve regurgitation). Understanding cardiac hypertrophy is critical to comprehending the mechanisms of heart development and treatment of heart disease. However, the major molecular event that occurs during physiological or pathological hypertrophy is the dynamic process of sarcomeric addition, and it has not been observed...
February 10, 2016: Scientific Reports
Biruta Kierdaszuk, Mariusz Berdynski, Piotr Palczewski, Marek Golebiowski, Cezary Zekanowski, Anna Maria Kaminska
INTRODUCTION: Sporadic inclusion body myositis (sIBM) is one of the most common myopathies in patients above 50 years of age. Its progressive course finally leads to immobilisation, and no effective therapy exists. Its pathogenesis includes both degenerative and inflammatory processes, however, its direct causes remain unknown. Therefore, a possible genetic background of the disease must also be considered. MATERIAL AND METHODS: Here we report on twelve patients: eight with sporadic inclusion body myositis and four with other myopathies with rimmed vacuoles in muscle biopsy...
2015: Folia Neuropathologica
Katharina Wassilew, Denis Terziev, Georgi Wassilew, Günther Fitzl, Karsten Frölich, Reinhard Kandolf, Andreas Fried
AIM: The present study aims to analyze the differences in ultrastructural changes between right ventricular myocardium in clinically determined grades of heart failure (HF) [New York Heart Association (NYHA) classes I-IV] and their value in the routine diagnostic setting. METHODS: We investigated consecutive right ventricular endomyocardial biopsies of 12 patients presenting with HF (49±11.2years; male=10) by light microscopy and ultrastructural morphometric analysis...
January 2016: Cardiovascular Pathology: the Official Journal of the Society for Cardiovascular Pathology
J P Meijer, R T Jaspers, J Rittweger, O R Seynnes, S Kamandulis, M Brazaitis, A Skurvydas, R Pišot, B Šimunič, M V Narici, H Degens
What is the central question of this study? Do the contractile properties of single muscle fibres differ between body-builders, power athletes and control subjects? What is the main finding and its importance? Peak power normalized for muscle fibre volume in power athletes is higher than in control subjects. Compared with control subjects, maximal isometric tension (normalized for muscle fibre cross-sectional area) is lower in body-builders. Although this difference may be caused in part by an apparent negative effect of hypertrophy, these results indicate that the training history of power athletes may increase muscle fibre quality, whereas body-building may be detrimental...
November 2015: Experimental Physiology
Christopher M Kramer, Evan Appelbaum, Milind Y Desai, Patrice Desvigne-Nickens, John P DiMarco, Matthias G Friedrich, Nancy Geller, Sarahfaye Heckler, Carolyn Y Ho, Michael Jerosch-Herold, Elizabeth A Ivey, Julianna Keleti, Dong-Yun Kim, Paul Kolm, Raymond Y Kwong, Martin S Maron, Jeanette Schulz-Menger, Stefan Piechnik, Hugh Watkins, William S Weintraub, Pan Wu, Stefan Neubauer
Hypertrophic cardiomyopathy (HCM) is the most common monogenic heart disease with a frequency as high as 1 in 200. In many cases, HCM is caused by mutations in genes encoding the different components of the sarcomere apparatus. Hypertrophic cardiomyopathy is characterized by unexplained left ventricular hypertrophy, myofibrillar disarray, and myocardial fibrosis. The phenotypic expression is quite variable. Although most patients with HCM are asymptomatic, serious consequences are experienced in a subset of affected individuals who present initially with sudden cardiac death or progress to refractory heart failure...
August 2015: American Heart Journal
Jianming Jiang, Patrick G Burgon, Hiroko Wakimoto, Kenji Onoue, Joshua M Gorham, Caitlin C O'Meara, Gregory Fomovsky, Bradley K McConnell, Richard T Lee, J G Seidman, Christine E Seidman
Homozygous cardiac myosin binding protein C-deficient (Mybpc(t/t)) mice develop dramatic cardiac dilation shortly after birth; heart size increases almost twofold. We have investigated the mechanism of cardiac enlargement in these hearts. Throughout embryogenesis myocytes undergo cell division while maintaining the capacity to pump blood by rapidly disassembling and reforming myofibrillar components of the sarcomere throughout cell cycle progression. Shortly after birth, myocyte cell division ceases. Cardiac MYBPC is a thick filament protein that regulates sarcomere organization and rigidity...
July 21, 2015: Proceedings of the National Academy of Sciences of the United States of America
Anastasia Karabina, Katarzyna Kazmierczak, Danuta Szczesna-Cordary, Jeffrey R Moore
Familial hypertrophic cardiomyopathy (HCM) is characterized by left ventricular hypertrophy and myofibrillar disarray, and often results in sudden cardiac death. Two HCM mutations, N47K and R58Q, are located in the myosin regulatory light chain (RLC). The RLC mechanically stabilizes the myosin lever arm, which is crucial to myosin's ability to transmit contractile force. The N47K and R58Q mutations have previously been shown to reduce actin filament velocity under load, stemming from a more compliant lever arm (Greenberg, 2010)...
August 15, 2015: Archives of Biochemistry and Biophysics
Vikram Prasad, John N Lorenz, Valerie M Lasko, Michelle L Nieman, Wei Huang, Yigang Wang, David W Wieczorek, Gary E Shull
Null mutations in one copy of ATP2A2, the gene encoding sarco/endoplasmic reticulum Ca(2+)-ATPase isoform 2 (SERCA2), cause Darier disease in humans, a skin condition involving keratinocytes. Cardiac function appears to be unimpaired in Darier disease patients, with no evidence that SERCA2 haploinsufficiency itself causes heart disease. However, SERCA2 deficiency is widely considered a contributing factor in heart failure. We therefore analyzed Atp2a2 heterozygous mice to determine whether SERCA2 haploinsufficiency can exacerbate specific heart disease conditions...
2015: BioMed Research International
Manuela Lavorato, Tai-Qin Huang, Venkat Ramesh Iyer, Stefano Perni, Gerhard Meissner, Clara Franzini-Armstrong
In cardiac muscle, calmodulin (CaM) regulates the activity of several membrane proteins involved in Ca(2+) homeostasis (CaV1.2; RyR2, SERCA2, PMCA). Three engineered amino acid substitutions in the CaM binding site of the cardiac ryanodine receptor (RyR2) in mice (Ryr2 (ADA/ADA) ) strongly affect cardiac function, with impaired CaM inhibition of RyR2, reduced SR Ca(2+) sequestration, and early cardiac hypertrophy and death (Yamaguchi et al., J Clin Invest 117:1344-1353, 2007). We have examined the ultrastructure and RyR2 immunolocalization in WT and Ryr2 (ADA/ADA) hearts at ~10 days after birth...
April 2015: Journal of Muscle Research and Cell Motility
Leah Cannon, Ze-Yan Yu, Tadeusz Marciniec, Ashley J Waardenberg, Siiri E Iismaa, Vesna Nikolova-Krstevski, Elysia Neist, Monique Ohanian, Min Ru Qiu, Stephen Rainer, Richard P Harvey, Michael P Feneley, Robert M Graham, Diane Fatkin
BACKGROUND: Hypertrophic cardiomyopathy (HCM) is caused by mutations in sarcomere protein genes, and left ventricular hypertrophy (LVH) develops as an adaptive response to sarcomere dysfunction. It remains unclear whether persistent expression of the mutant gene is required for LVH or whether early gene expression acts as an immutable inductive trigger. OBJECTIVES: The aim of this study was to use a regulatable murine model of HCM to study the reversibility of pathological LVH...
February 17, 2015: Journal of the American College of Cardiology
G Py, C Ramonatxo, P Sirvent, A M J Sanchez, A G Philippe, A Douillard, O Galbès, C Lionne, A Bonnieu, A Chopard, O Cazorla, A Lacampagne, R B Candau
Clenbuterol is a β2 -adrenergic receptor agonist known to induce skeletal muscle hypertrophy and a slow-to-fast phenotypic shift. The aim of the present study was to test the effects of chronic clenbuterol treatment on contractile efficiency and explore the underlying mechanisms, i.e. the muscle contractile machinery and calcium-handling ability. Forty-three 6-week-old male Wistar rats were randomly allocated to one of six groups that were treated with either subcutaneous equimolar doses of clenbuterol (4 mg kg(-1) day(-1) ) or saline solution for 9, 14 or 21 days...
April 15, 2015: Journal of Physiology
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