Decreased proportion of type I myofibers in skeletal muscle of dogs with chronic heart failure.

Sabbah, Hani N.; Hansen-Smith, Fay M.; Sharov, Victor G.; Kono, Tatsuji; Lesch, Michael; Gengo, Peter J.; Steffen, Robert P.; Levine, T. Barry; Goldstein, Sidney

doi:10.1161/01.cir.87.5.1729

Cited by 47 publications

(39 citation statements)

References 26 publications

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“…2,3,5,7,9,11,22 We report here a reduced number of capillaries and changes in MHC expression in SOL from CHF rats that consist of decreased type I MHC expression and increased fast-type IIa MHC expression. Fibers generally express a whole set of contractile proteins of a specific type, including regulatory proteins of the thin filament.…”

Section: Contractile Functionmentioning

confidence: 63%

Heart Failure Affects Mitochondrial but Not Myofibrillar Intrinsic Properties of Skeletal Muscle

et al. 2000

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Background-Congestive heart failure (CHF) induces abnormalities in skeletal muscle that are thought to in part explain exercise intolerance. The aim of the present study was to determine whether these changes actually result in contractile or metabolic functional alterations and whether they are muscle type specific. Methods and Results-With a rat model of CHF (induced by aortic banding), we studied mitochondrial function, mechanical properties, and creatine kinase (CK) compartmentation in situ in permeabilized fibers from soleus (SOL), an oxidative slow-twitch muscle, and white gastrocnemius (GAS), a glycolytic fast-twitch muscle. Animals were studied 7 months after surgery, and CHF was documented on the basis of anatomic data. Alterations in skeletal muscle phenotype were documented with an increased proportion of fast-type fiber and fast myosin heavy chain, decreased capillary-to-fiber ratio, and decreased citrate synthase activity. Despite a slow-to-fast phenotype transition in SOL, no change was observed in contractile capacity or calcium sensitivity. However, muscles from CHF rats exhibited a dramatic decrease in oxidative capacities (oxygen consumption per gram of fiber dry weight) of 35% for SOL and 45% for GAS (PϽ0.001). Moreover, the regulation of respiration with ADP and mitochondrial CK and adenylate kinase was impaired in CHF SOL. Mitochondrial CK activity and content (Western blots) were dramatically decreased in both muscles. Conclusions-CHF results in alterations in both mitochondrial function and phosphotransfer systems but unchanged myofibrillar function in skeletal muscles, which suggests a myopathy of metabolic origin in CHF. (Circulation.

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Section: Contractile Functionmentioning

confidence: 63%

Heart Failure Affects Mitochondrial but Not Myofibrillar Intrinsic Properties of Skeletal Muscle

et al. 2000

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“…4). The slow oxidative fibers and functional mitochondria are relatively resistant to the progressive myonecrosis that occurs with advancing age in Duchenne's muscular dystrophy -characterized by a lack of dystrophin -and in individuals that suffer congestive heart failure (Chin et al, 1998;Ljubicic et al, 2011;Sabbah et al, 1993); therefore, the discovery of a factor that promotes a fast-to-slow fiber switch in individuals will be important to decrease morbidity and improve quality of life. Therefore, NRIP could be a good target for future therapeutic treatment in muscular dystrophy, chronic diseases that are characterized by physical inability and/or loss of muscle mass, and ageing.…”

Section: Discussionmentioning

confidence: 99%

NRIP is a novel Z-disc protein to activate calmodulin signaling for skeletal muscle contraction and regeneration

Chen

Yan

et al. 2015

Journal of Cell Science

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Nuclear receptor interaction protein (NRIP, also known as DCAF6 and IQWD1) is a Ca 2+ -dependent calmodulin-binding protein.In this study, we newly identify NRIP as a Z-disc protein in skeletal muscle. NRIP-knockout mice were generated and found to have reduced muscle strength, susceptibility to fatigue and impaired adaptive exercise performance. The mechanisms of NRIP-regulated muscle contraction depend on NRIP being downstream of Ca 2+ signaling, where it stimulates activation of both 'calcineurin-nuclear factor of activated T-cells, cytoplasmic 1' (CaN-NFATc1; also known as NFATC1) and calmodulin-dependent protein kinase II (CaMKII) through interaction with calmodulin (CaM), resulting in the induction of mitochondrial activity and the expression of genes encoding the slow class of myosin, and in the regulation of Ca 2+ homeostasis through the internal Ca 2+ stores of the sarcoplasmic reticulum. Moreover, NRIP-knockout mice have a delayed regenerative capacity. The amount of NRIP can be enhanced after muscle injury and is responsible for muscle regeneration, which is associated with the increased expression of myogenin, desmin and embryonic myosin heavy chain during myogenesis, as well as for myotube formation. In conclusion, NRIP is a novel Z-disc protein that is important for skeletal muscle strength and regenerative capacity.

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“…However, in a canine model of chronic heart failure, the proportion of slow-twitch fibers is decreased. 150 This could not be attributed to changes in capillary density or muscle fiber destruction. Similar changes in fiber type (combined with exercise intolerance) are seen in human heart failure, although here there may also be fiber loss and changes in capillary density (reviewed in Reference 151).…”

Section: Calcineurin and Specification Of Skeletal Muscle Fiber Typementioning

confidence: 99%

Signaling in Myocardial Hypertrophy

Sugden

1999

Circulation Research

180

126

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C ardiac (ventricular) hypertrophy is an important adaptive response in vivo that (at least in the shorter term) allows the organism to maintain or increase its cardiac output. Global ventricular hypertrophy is a recognized response to increased pressure or volume work (reviewed in Reference 1), with increased myofibrillogenesis and sarcomere deposition being cardinal features. Although global hypertrophy is clinically important, probably the most significant form of cardiac hypertrophy in terms of patient numbers is the localized hypertrophy of the ventricular wall that may follow loss of myocardium after a survivable myocardial infarct. In the early stages, both global and localized hypertrophy may resemble the readily reversible, nonfibrotic "physiological" hypertrophy that develops after repeated endurance exercise. In the longer term, beneficial, "compensated" hypertrophy may decay into maladaptive "decompensated" hypertrophy and heart failure (reviewed in References 2 and 3) with diminished coronary flow reserve and increased risk of lethal arrhythmias. Although some aspects of the maladapted state are probably intrinsic to the myocyte [eg, prolongation of the action potential and Ca 2ϩ transient (reviewed in References 4 and 5)], other factors (increased fibrosis and mismatch between O 2 supply and demand) are also probably involved in decompensation.The predominating view is that mammalian ventricular myocytes lose their capacity for cell division during the perinatal period and are thus terminally differentiated cells, although this is still a matter of some dispute (reviewed in References 6 and 7). In contrast, other cells in the heart (endothelial cells, fibroblasts, and smooth muscle cells) retain their mitotic capacity. Although ventricular myocytes are not the only cell type involved in the overall hypertrophic response, much of the ventricular enlargement or remodeling is attributable to their hypertrophy. The identities of signaling pathways that couple the demand for increased contractile power to increased myocyte growth and altered gene expression have been actively investigated for many years. Protein phosphorylation (catalyzed principally by Ser-/Thr-or Tyrspecific protein kinases) and phosphoprotein dephosphorylation (catalyzed by phosphoprotein phosphatases) play central roles in the regulation of many cellular events, including growth and cell division, and it is widely believed that these processes participate in myocyte hypertrophy.From the broad point of view, 2 hypotheses of hypertrophy have been proposed, which are the extrinsic and the intrinsic hypotheses. The former maintains that myocyte hypertrophy results from extracellular factors ( Table 1) that are either of a neuroendocrine origin (eg, the catecholamines) or are synthesized and released locally by the myocytes and nonmyocytes in the heart (eg, endothelin-1 [ET-1] and angiotensin II [Ang II]). The intrinsic hypothesis maintains that changes originating within the myocyte are responsible for hypertrophy. Because of its well-e...

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Decreased proportion of type I myofibers in skeletal muscle of dogs with chronic heart failure.

Cited by 47 publications

References 26 publications

Heart Failure Affects Mitochondrial but Not Myofibrillar Intrinsic Properties of Skeletal Muscle

Heart Failure Affects Mitochondrial but Not Myofibrillar Intrinsic Properties of Skeletal Muscle

NRIP is a novel Z-disc protein to activate calmodulin signaling for skeletal muscle contraction and regeneration

Signaling in Myocardial Hypertrophy

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