ライフサイエンスコーパス: cardiac muscle

1 role in matching energy supply and demand in cardiac muscle.

2 It also has an anti-inflammatory role in cardiac muscle.

3 by progressive degeneration of skeletal and cardiac muscle.

4 Pip peptide-AOs demonstrate high activity in cardiac muscle.

5 eas alphaCAA and alphaSKA are coexpressed in cardiac muscle.

6 the force and kinetics of twitches in living cardiac muscle.

7 s potential impact on the function of intact cardiac muscle.

8 highly expressed in human adult skeletal and cardiac muscle.

9 structures essential to the pump function of cardiac muscle.

10 wo Gtl2-Dio3 miRNAs, miR-410 and miR-495, in cardiac muscle.

11 rom troponin C and the rate of relaxation in cardiac muscle.

12 t and protein carbonylation were measured in cardiac muscle.

13 least four Hax-1 transcripts in healthy rat cardiac muscle.

14 mental, and regulatory roles in skeletal and cardiac muscle.

15 , a 65-kDa protein expressed in skeletal and cardiac muscle.

16 ribed to SCN5A, which is highly expressed in cardiac muscle.

17 ost appendages and injured organs, including cardiac muscle.

18 active alternative strategy for regenerating cardiac muscle.

19 ular lipid accumulation in both skeletal and cardiac muscle.

20 eptors, and termination of calcium sparks in cardiac muscle.

21 generation and necrosis of both skeletal and cardiac muscle.

22 Nav1.5 drive electrogenesis in skeletal and cardiac muscle.

23 itor cells develop into strongly contractile cardiac muscle.

24 ence of force-pCa relations in demembranated cardiac muscle.

25 Here, we characterize this pathway in cardiac muscle.

26 Phospholemman oligomers exist in cardiac muscle.

27 iomyocytes to proliferate and replenish lost cardiac muscle.

28 , and restores function in both skeletal and cardiac muscle.

29 um sensitivity and contractile efficiency of cardiac muscle.

30 2 months in skeletal muscle, but shorter in cardiac muscle.

31 impacted muscle compliance in Fhl1 knock-out cardiac muscle.

32 uired for excitation-contraction coupling in cardiac muscle.

33 normal levels in skeletal muscle, and 15% in cardiac muscle.

34 ting contractility and Ca(2+) sensitivity of cardiac muscle.

35 ed the effect of HSSTnT on the regulation of cardiac muscle.

36 esult in excessive accumulation of lipids in cardiac muscle.

37 he coupling of excitation and contraction in cardiac muscle.

38 rcomere function to augment contractility in cardiac muscle.

39 stic sarcoplasmic inclusions in skeletal and cardiac muscle.

40 ease of complex III activity in skeletal and cardiac muscle.

41 thesis defects were confined to skeletal and cardiac muscle.

42 e c oxidase-deficient fibres in skeletal and cardiac muscle.

43 role in matching energy supply and demand in cardiac muscle.

44 acterized by impairment of both skeletal and cardiac muscle.

45 unds that differentially affect skeletal and cardiac muscles.

46 the structure and physiology of skeletal and cardiac muscles.

47 phin expression in skeletal, respiratory and cardiac muscles.

48 sensitivity in streptozotocin (STZ) diabetic cardiac muscles.

49 itation-contraction coupling of skeletal and cardiac muscles.

50 surements in ventricular myocytes and intact cardiac muscles.

51 plasmic reticulum (SR) lumen in skeletal and cardiac muscles.

52 ntly expressed at sarcomeres in skeletal and cardiac muscles.

53 0% activation (Ca(50)) in intact and skinned cardiac muscles.

54 in several splicing defects in skeletal and cardiac muscles.

55 posite effects were observed in skeletal and cardiac muscles.

56 e of diverse tissues, including skeletal and cardiac muscles.

57 pression in autophagy-deficient skeletal and cardiac muscles.

58 xpression of dystrophin in both skeletal and cardiac muscles.

59 In cardiac muscle, a subpopulation of phospholemman with a

60 t zebrafish and neonatal mice can regenerate cardiac muscle after injury, suggesting that latent rege

61 levels in patient fibroblasts, skeletal and cardiac muscle, although mitochondrial protein synthesis

62 cardiac reprogramming factors generates new cardiac muscle and improved heart function after myocard

63 en shown to increase the power output of the cardiac muscle and is currently in clinical trials for t

64 yocarditis is an inflammatory disease of the cardiac muscle and is mainly caused by viral infections.

65 otein expressed ubiquitously in skeletal and cardiac muscle and is traditionally considered to functi

66 e abundantly found in human skeletal muscle, cardiac muscle and neuronal cells having numerous proper

67 e peptides, most notably by phospholamban in cardiac muscle and sarcolipin in skeletal muscle.

68 ly shown that FKBP12 associates with RyR2 in cardiac muscle and that it modulates RyR2 function diffe

69 ) has enhanced capsid-associated tropism for cardiac muscle and the ability to cross the blood-brain

70 and -2 are highly expressed in skeletal and cardiac muscle and together with SUN (Sad1p/UNC84)-domai

71 t is predominantly expressed in skeletal and cardiac muscles and belongs to the AC group of proteins,

72 ne that lead to degeneration of skeletal and cardiac muscles and to chronic inflammation.

73 DMD leads to degeneration of skeletal and cardiac muscles and to chronic inflammation.

74 s (IC50) estimated at 130, 19, and 9 microM (cardiac muscle) and 104, 13, and 5 microM (SkM SR).

75 increase of glucose uptake into skeletal and cardiac muscle, and a twofold increase in insulin signal

76 and very large (Ttn: 106 kb) transcripts in cardiac muscle, and fast and slow skeletal muscles ident

77 le in modulating mitochondrial metabolism in cardiac muscle, and Grx2 deficiency leads to pathology.

78 n when pre-established, in both skeletal and cardiac muscle, and improves skeletal muscle function.

79 omere proteins (including TNNI3 [troponin I, cardiac muscle]) and ion channels (including Kir2.1) in

80 (2+)-release channels (RyRs) of skeletal and cardiac muscle are essential for Ca(2+) release from the

81 nosine 5'-triphosphate (dATP) can be used by cardiac muscle as an alternative energy substrate for my

82 lated differences in dystrophic skeletal and cardiac muscles as compared with their age-matched contr

83 eloped to model extreme mitochondrial Kac in cardiac muscle, as confirmed by quantitative acetyl-prot

84 een traditionally viewed as a disease of the cardiac muscle associated with systemic inflammation.

85 all response to this stress may culminate in cardiac muscle atrophy.

86 d the increase in diffuse reflectance of the cardiac muscle beneath the endocardial layer.

87 ificant not only because LDA is prominent in cardiac muscle but also because it contributes to the Fr

88 tly modulating actin thin filament length in cardiac muscle by binding monomeric actin and limiting i

89 Most LMNA mutations affect skeletal and cardiac muscle by mechanisms that remain incompletely un

90 cardiomyopathies remains unclear, improving cardiac muscle Ca(2+) sensitivity through either pharmac

91 ile therapeutic strategy to restore diseased cardiac muscle Ca(2+) sensitivity.

92 eart to work at a level much higher than the cardiac muscle can handle.

93 with heart failure, a condition with reduced cardiac muscle cBIN1, both of which support cBIN1 releas

94 ly, few methods can predict the state of the cardiac muscle cell and its metabolic conditions during

95 MAPK superfamily that is implicated in human cardiac muscle cell death from oxidative stress, based o

96 enrichment > 2) were identified, including 'cardiac muscle cell differentiation'.

97 rced expression of POPDC1(S201F) in a murine cardiac muscle cell line (HL-1) increased hyperpolarizat

98 n signaling and function in the skeletal and cardiac muscle cell.

99 the contractile strains produced by beating cardiac muscle cells can be optimized by substrate stiff

100 eton; their disruption within epithelial and cardiac muscle cells cause skin-blistering diseases and

101 Cardiac muscle cells have an intrinsic ability to sense

102 Cardiac muscle cells lack regenerative capacity in postn

103 potentially for optimizing communication of cardiac muscle cells through gap junctions.

104 e repair process, especially in skeletal and cardiac muscle cells, in which contraction-induced mecha

105 produced keratinocytes, smooth muscle cells, cardiac muscle cells, neurons and glial cells.

106 In cardiac muscle cells, spontaneous store overload-induced

107 barrier function and spontaneous beating of cardiac muscle cells, which are important functions of c

108 orm physical and functional connections with cardiac muscle cells.

109 Ca2+]i, regulate the contractile function of cardiac muscle cells.

110 l role in excitation-contraction coupling in cardiac muscle cells.

111 in with a role in the repair of skeletal and cardiac muscle cells.

112 structural substates for SERCA expressed in cardiac muscle cells.

113 ) release through RyRs in neuronal cells and cardiac muscle cells.

114 lcNAcylation modulates DRP1 functionality in cardiac muscle cells.

115 te or inhibit contractility in demembranated cardiac muscle cells.

116 t failure (HF), energy metabolism pathway in cardiac muscle changes from fatty acid beta-oxidation to

117 For cardiac-muscle channels (NaV1.5), reported effects from

118 Similarly, cardiac muscle (CM)-specific Plin5 overexpression (CM-Pl

119 y muscles was also restored in CRISPR-edited cardiac muscles compared with untreated controls.

120 The cardiac muscle comprises dynamically interacting compone

121 tailed mechanisms of drug-induced effects on cardiac muscle contractility.

122 into the modulatory role of this protein in cardiac muscle contractility.

123 nd explain the importance of alpha2beta2 for cardiac muscle contractility.

124 innovative therapeutic approaches to enhance cardiac muscle contractility.

125 e (SERCA) pump is a major regulatory axis in cardiac muscle contractility.

126 ,K-ATPase alpha2 subunit plays a key role in cardiac muscle contraction by regulating intracellular C

127 Myocardial depolarization leading to cardiac muscle contraction is reflected by the amplitude

128 Cardiac muscle contraction is triggered by calcium bindi

129 ptor interaction, oxidative phosphorylation, cardiac muscle contraction, Alzheimer's disease, Parkins

130 ding myosin, the molecular motor that powers cardiac muscle contraction, and its accessory protein, c

131 to its central role as the Ca(2+) sensor for cardiac muscle contraction, troponin C (TnC) stands out

132 that interacts with troponin I and initiates cardiac muscle contraction.

133 is a key molecule in the regulation of human cardiac muscle contraction.

134 rk for understanding cMyBP-C's modulation of cardiac muscle contraction.

135 ed muscle thick filaments and a modulator of cardiac muscle contraction.

136 n cardiomyocytes and determines the force of cardiac muscle contraction.

137 actin and myosin that allows fine tuning of cardiac muscle contraction.

138 role in the activation of calcium-dependent cardiac muscle contraction.

139 r Mlc2 (Mlc2v) phosphorylation in regulating cardiac muscle contraction.

140 rdiac TnT are critical for the regulation of cardiac muscle contraction.

141 l changes, and whether these residues affect cardiac muscle contraction.

142 smyd1b mutant, which exhibited skeletal and cardiac muscle defects, leading to early embryonic letha

143 urologic function as well as in skeletal and cardiac muscle defects.

144 flammation substantially affect skeletal and cardiac muscle degeneration in Duchenne muscular dystrop

145 aging of Drosophila skeletal muscle, but not cardiac muscle, despite the strong evolutionary conserva

146 an essential role in zebrafish skeletal and cardiac muscle development.

147 programs critical in smooth muscle (SM) and cardiac muscle development.

148 We observe enrichment for cardiac muscle developmental/contractile and cytoskeleta

149 The deletion of VEGF in cardiac muscle did not affect cardiac output.

150 ty, most likely due to the role of miR-1a in cardiac muscle differentiation.

151 identify compounds that affect skeletal and cardiac muscle differently.

152 aveolae in endothelial cells of the lung and cardiac muscle disassemble in response to acute increase

153 in (DES) mutations cause severe skeletal and cardiac muscle disease with heterogeneous phenotypes.

154 iac function, and mutations in cMyBP-C cause cardiac muscle disease.

155 DES mutations cause severe skeletal and cardiac muscle diseases with heterogeneous phenotypes.

156 ed with increased prevalence of skeletal and cardiac muscle disorders, such as sarcopenia and cardiac

157 In Trpm4(-/-) mice, cardiac muscle displays an increased beta-adrenergic ino

158 s and is caused by the lack of oxygen within cardiac muscles due to an imbalance between oxygen suppl

159 ut the contractile properties of human fetal cardiac muscle during development.

160 chanical function and tissue organization in cardiac muscle during HF.

161 In cardiac muscle, dysferlin is located at the intercalated

162 ct on exercise performance, and skeletal and cardiac muscle dysfunction contributes to this deficienc

163 itric-oxide-signaling cascade that increases cardiac muscle elasticity.

164 -like fiber orientation in both skeletal and cardiac muscle, enabling scale up of tissue constructs t

165 cited by exercise in the autophagy deficient cardiac muscle enhances whole-body metabolism, at least

166 tors, ion channels critical for skeletal and cardiac muscle excitation-contraction coupling and synap

167 Upon activation, contraction of cardiac muscle expels blood into the circulation.

168 in Escherichia coli confirmed that the toad cardiac muscle expresses solely ssTnT, predominantly the

169 sufficient ability to replenish the damaged cardiac muscles, extensive research has been devoted tow

170 Cardiac muscle fiber mechanic studies demonstrate cross-

171 s a noted restoration in the architecture of cardiac muscle fibers and a reduction in the extent of f

172 tergent-skinned guinea pig (Cavia porcellus) cardiac muscle fibers in the absence and presence of 0.3

173 ng the preferential diffusion of water along cardiac muscle fibers using diffusion tensor cardiac mag

174 RfsT1-RcT2- and RcT1-RfsT2-reconstituted rat cardiac muscle fibers were captured by fitting the recru

175 conformational behavior of N-cTnC in skinned cardiac muscle fibers.

176 It can be observed in both skeletal and cardiac muscle fibers.

177 olism were assessed in saponin-permeabilized cardiac muscle fibers.

178 Cardiac muscle fibres from these mice contained approxim

179 licated a wide range of molecular targets in cardiac muscle for the major green tea catechin, (-)-epi

180 lation plays an important role in modulating cardiac muscle function and accelerating contraction.

181 vs. cardiac isoforms of either TnI or MHC on cardiac muscle function and contractile dynamics.

182 Myocardial mass is a key determinant of cardiac muscle function and hypertrophy.

183 n to be implicated in lung, reproductive and cardiac muscle function and in the cause of cancer.

184 ng mechanisms underlying titin regulation in cardiac muscle function is of critical importance given

185 Skeletal and cardiac muscle function, inflammation, regeneration, his

186 nsic in vivo movement and characteristics of cardiac muscle function.

187 ction pathways are critical for skeletal and cardiac muscle function.

188 ockout (tKO) mice] and assessed skeletal and cardiac muscle function.

189 Ca storage organelle, is critical for proper cardiac muscle function.

190 ell (SC) exhaustion and loss of skeletal and cardiac muscle function.

191 ing protein, are critical to maintain proper cardiac muscle function; however, the connection between

192 se of Ca from intracellular stores is key to cardiac muscle function; however, the molecular control

193 multiple cellular lineages, but its role in cardiac muscle has remained unclear.

194 Force and power in cardiac muscle have a known dependence on phosphorylatio

195 The contractile properties of human fetal cardiac muscle have not been previously studied.

196 he original GDF11 hypothesis in skeletal and cardiac muscle have not been validated by several indepe

197 muscle type than species: slow skeletal and cardiac muscles have wider Z-bands than fast skeletal mu

198 strophin degradation, preserved skeletal and cardiac muscle histology, and improved strength and hear

199 Cardiac muscle hypercontractility is a key pathophysiolo

200 dystrophin protein in skeletal myofibers and cardiac muscle, improvement of muscle biochemistry, and

201 (P6), representing a barrier to building new cardiac muscle in adults.

202 stained myosin filaments isolated from human cardiac muscle in the normal (undiseased) relaxed state.

203 ed subtomogram averaging of tomograms of rat cardiac muscle in which subtomograms are extracted and c

204 the importance of treating both skeletal and cardiac muscles in DMD therapy.

205 undamental force-generating machinery of the cardiac muscle, including beta-cardiac myosin.

206 n urine, histological review of skeletal and cardiac muscle indicates that the increased tissue accum

207 le disease mechanisms affecting skeletal and cardiac muscles, inflammatory cells, brain, and bone.

208 rt failure, in response to different initial cardiac muscle insults.

209 However, cardiac muscle is also a subtype of striated muscle and

210 term heart function, but whether regenerated cardiac muscle is biomechanically similar to native myoc

211 on of similar macromolecular organization in cardiac muscle is missing.

212 phosphorylated RLC region of myosin heads in cardiac muscle is primarily determined by an interaction

213 region of the myosin heads on activation of cardiac muscle is small; the RLC regions of most heads r

214 Contraction of skeletal and cardiac muscles is regulated by Ca(2+) binding to tropon

215 tions cause a severe phenotype especially in cardiac muscle leading to cardiomyopathy that can be let

216 ronic and progressive damage to skeletal and cardiac muscle leading to premature death.

217 In the heart, calcification of cardiac muscle leads to conduction system disturbances a

218 negative regulator of postnatal skeletal and cardiac muscle mass and modulates metabolic processes.

219 Thus, RLC phosphorylation in cardiac muscle may be regulated by two different protein

220 nction in cardiomyocytes and suggest that in cardiac muscle, MCL-1 also facilitates normal mitochondr

221 ory light chain (RLC) phosphorylation alters cardiac muscle mechanics is important because it is ofte

222 Thus, mtCU "hot spots" can be formed at the cardiac muscle mitochondria-SR associations via localiza

223 In cardiac muscle, mitochondrial ATP synthesis is driven by

224 In this review, we focus on mutations in the cardiac muscle molecular motor, myosin, and its associat

225 tension and the time course of relaxation in cardiac muscle myofibrils.

226 omecamtiv mecarbil (OM) specifically targets cardiac muscle myosin and is known to enhance cardiac mu

227 tivated ATPase activity of fast skeletal and cardiac muscle myosin II, inhibition of skeletal muscle

228 atomical location affected: skeletal muscle, cardiac muscle, neuromuscular junction, peripheral nerve

229 he marked increase in ATGL protein levels in cardiac muscle of CGI-58KOM mice was unable to compensat

230 e exercise induces autophagy in skeletal and cardiac muscle of fed mice.

231 e the migration of gammadelta T cells to the cardiac muscle of mdx mice and to characterize their phe

232 Here we report an exception that the cardiac muscle of toad (Bufo) expresses exclusively slow

233 aling, reduced Cthrc1 levels in skeletal and cardiac muscles of mice, representing DMD, CMD, and dysf

234 repeat containing 1 (Cthrc1) in skeletal and cardiac muscles of mice, representing Duchenne and conge

235 in expression was lower in both skeletal and cardiac muscles of tKO mice.

236 MR) techniques, we compared the skeletal and cardiac muscles of two different dystrophic mouse models

237 Injury to the cardiac muscle often leads to heart failure due to the l

238 human-induced pluripotent stem cell-derived cardiac muscle patch (hCMP), which was subsequently eval

239 ac flow characteristics and relating them to cardiac muscle performance in young adults.

240 ardiac muscle myosin and is known to enhance cardiac muscle performance, yet its impact on human card

241 inhibitor (sildenafil) improves skeletal and cardiac muscle performance.

242 urdles such as extremely low efficacy in the cardiac muscle, poor cellular uptake and relatively rapi

243 on of cryoablation lesions in blood-perfused cardiac muscle preparations and revealed similarities an

244 High-alanine TnT-containing cardiac muscle preparations had increased Ca(2+) sensiti

245 uman cTnC variant into permeabilized porcine cardiac muscle preparations significantly decreases the

246 m the sarcoplasmic reticulum of skeletal and cardiac muscle preparations, its mechanism of action has

247 ird clonal population of common skeletal and cardiac muscle progenitor cells within cardiopharyngeal

248 c is essential to activate both skeletal and cardiac muscle programs.

249 nese quail myoglobin was isolated from quail cardiac muscles, purified using ammonium sulphate precip

250 In addition to its known effects on cardiac muscle, recent in vitro and in vivo evidence hig

251 iPs engrafted and repaired both skeletal and cardiac muscle, reducing functional defects.

252 (ECM) directs cell activities essential for cardiac muscle regeneration.

253 ic cardiomyopathy, characterized by impaired cardiac muscle relaxation and force development.

254 for example, myosin light chain-2 [MLC2]) in cardiac muscle remain poorly understood.

255 s capable of recovering or replacing damaged cardiac muscle require physiologically relevant environm

256 els that are highly enriched in skeletal and cardiac muscle, respectively, where they play an essenti

257 ype I (RyR1) and II (RyR2) from skeletal and cardiac muscle, respectively.

258 ~50% decrease in capillaries in skeletal and cardiac muscle, respectively.

259 Cardiac muscle restitution, or true regeneration, is an

260 se A (PKA) phosphorylates class IIa HDACs in cardiac muscle, resulting in HDAC nuclear accumulation,

261 skeletal muscle, and L-type Ca(2+) entry in cardiac muscle, revealing a mechanism by which TCS weake

262 dentical to the 2460-2495 segment within the cardiac muscle RyR isoform (RyR2) central domain.

263 In cardiac muscle, SERCA is regulated by phospholamban (PLB

264 ovascular system (such as endothelial cells, cardiac muscle, smooth muscle, inflammatory cells, and f

265 locus reveal a putative causal variant in a cardiac muscle specific regulatory region activated duri

266 everal tissues; yet the role of skeletal and cardiac muscle-specific autophagy on the benefits of exe

267 lar system and present evidence supporting a cardiac muscle-specific effect of n-6 PUFAs.

268 Skeletal- and cardiac-muscle-specific SRF knockouts resulted in signif

269 single cardiac myofibrils and multicellular cardiac muscle strips of three HCM patients with the R40

270 Understanding the time course of human fetal cardiac muscle structure and contractile maturation can

271 n, ventricular wall thickness, angiogenesis, cardiac muscle survival, and reducing fibrosis and infla

272 orm to investigate extracellular signals for cardiac muscle survival, substantiating human cardioprot

273 Here, using the cardiac muscle system, we demonstrate that nuclear recep

274 In mammalian skeletal and cardiac muscle, the Tm is expressed from two separate ge

275 ined troponin organization on native relaxed cardiac muscle thin filaments by applying single particl

276 whereas MV is mainly expressed in smooth and cardiac muscle tissue.

277 In striated muscle, including involuntary cardiac muscle, Tm regulates muscle contraction by coupl

278 sfunction and blunted lusitropic response of cardiac muscle to beta-adrenergic stimulation indicate a

279 brillin 1 in the physiological adaptation of cardiac muscle to elevated workload.

280 dystrophin protein expression in dystrophic cardiac muscles to a level approaching 40%.

281 ately in the thick and thin filaments of rat cardiac muscle, to elucidate that mechanism.

282 During the postnatal period in mammals, the cardiac muscle transitions from hyperplasic to hypertrop

283 in this allosteric/cooperative mechanism is cardiac muscle troponin T (cTnT), the central region (CR

284 anisms produced early defects in the rate of cardiac muscle twitch relaxation and ventricular torsion

285 Our analyses suggest that CIA is present in cardiac muscle under normal conditions and that its modu

286 ation and relaxation kinetics of human fetal cardiac muscle under well-controlled conditions.

287 ully isolated thick filaments from zebrafish cardiac muscle, using a procedure similar to those for m

288 esistance in chow-fed mice with skeletal and cardiac muscle VEGF deletion (mVEGF(-/-)) and wild-type

289 However, neither extraocular nor cardiac muscle was affected in double-knockout animals.

290 mice, glycogen accumulation in skeletal and cardiac muscles was not affected, but glycogen content i

291 dystrophin loss that results in skeletal and cardiac muscle weakening and early death.

292 essed as the greatest in skeletal muscle and cardiac muscle where it localized to the nucleus.

293 nt a model of Ca-regulated thin filaments in cardiac muscle where tropomyosin is treated as a continu

294 SPEG is present in cardiac muscle, where it plays a critical role; therefor

295 applied load, in qualitative agreement with cardiac muscle, which contracts with a velocity inversel

296 OM is known to enhance force generation in cardiac muscle while it inhibits the myosin power stroke

297 ic KKAy mice by increasing glucose uptake in cardiac muscle, white adipose tissue, and brown adipose

298 racterized MLCK, MLCK4, is also expressed in cardiac muscle with high catalytic domain sequence simil

299 exhibit abundant expression in skeletal and cardiac muscle with very low levels in SMC-containing ti

300 OBEC2 mRNA was most abundant in skeletal and cardiac muscle, with relatively low expression in the go