ライフサイエンスコーパス: cardiac myocyte

1 increase in size occurs at the level of the cardiac myocyte.

2 s specificity to calcineurin function in the cardiac myocyte.

3 res during differentiation and maturation of cardiac myocytes.

4 l calcium concentration were observed in rat cardiac myocytes.

5 tracrine control of respiration by NO within cardiac myocytes.

6 nished delayed aftercontractions in HRC null cardiac myocytes.

7 y couples the cycling of Ca(2+) and Na(+) in cardiac myocytes.

8 otein is mechanically active in skeletal and cardiac myocytes.

9 y to cell death in embryonic fibroblasts and cardiac myocytes.

10 e form of HCO3(-), impairs O2/CO2 balance in cardiac myocytes.

11 cium and mitochondria-dependent apoptosis in cardiac myocytes.

12 channel function is exquisitely regulated in cardiac myocytes.

13 ural backbone for coordinated contraction of cardiac myocytes.

14 in of beta-adrenergic stimulation in beating cardiac myocytes.

15 to study the biology of newly forming adult cardiac myocytes.

16 ophysiology in left versus right ventricular cardiac myocytes.

17 rodomain Ca(2+)-contraction coupling in live cardiac myocytes.

18 for driving maturation of stem cell-derived cardiac myocytes.

19 zation are crucial in the proper function of cardiac myocytes.

20 ide new insights into mechanotransduction in cardiac myocytes.

21 atastrophe, a previously unreported event in cardiac myocytes.

22 arvalbumin's EF-hand motif alter function of cardiac myocytes.

23 ncreases heart rate and the contractility of cardiac myocytes.

24 l strain at the subsarcomere level in living cardiac myocytes.

25 strophe was also confirmed in isolated adult cardiac myocytes.

26 lecule that rescues the disease phenotype in cardiac myocytes.

27 on depolarized mitochondria in neonatal rat cardiac myocytes.

28 ndent ryanodine receptor activation in adult cardiac myocytes.

29 romatin state on transcriptional activity in cardiac myocytes.

30 ht into the regulation of gene expression in cardiac myocytes.

31 onents of the adaptive ER stress response in cardiac myocytes.

32 293 cells expressing HERG channel and native cardiac myocytes.

33 n beta-adrenoreceptor signal transduction in cardiac myocytes.

34 n contrast to results obtained from purified cardiac myocytes.

35 disrupts excitation-contraction coupling in cardiac myocytes.

36 rganization and cellular stress responses in cardiac myocytes.

37 merged as a component of Ca(2+) signaling in cardiac myocytes.

38 and disturbs mitochondrial ultrastructure in cardiac myocytes.

39 nses have been studied in detail in isolated cardiac myocytes.

40 1+/-1.5 Mbp were identified in control human cardiac myocytes.

41 ld type) or a mutant LMNA (D300N) protein in cardiac myocytes.

42 n or fission and are seemingly static within cardiac myocytes.

43 ts function is during hypertrophic growth of cardiac myocytes.

44 t is triggered in post-mitotic cells such as cardiac myocytes.

45 n of beta1 adrenergic receptors (betaARs) on cardiac myocytes.

46 expression in response to cardiac stress in cardiac myocytes.

47 electron microscopy we identified, in adult cardiac myocytes, a Na(V)1.5 subpopulation in close prox

48 In cardiac myocytes, action potentials are initiated by an

49 sitive potassium channels (KATP channels) in cardiac myocytes adjust contractile function to compensa

50 subcellular distribution and preservation in cardiac myocytes after cell isolation are not well docum

51 activity within the myofilament fraction of cardiac myocytes after exposure to NCA revealed activati

52 at these candidate loci in neonatal cultured cardiac myocytes after in utero exposure to diesel exhau

53 rt IGF-1 as a potential strategy to increase cardiac myocyte and coronary vascular endowment at birth

54 ial duration and mitochondrial energetics to cardiac myocyte and whole-heart contractile function.

55 he cytoplasm and the mitochondrial matrix in cardiac myocytes and can be exploited to answer question

56 atment elevated both cAMP and cGMP levels in cardiac myocytes and cardiac fibroblasts, consistent wit

57 om comparing static mitochondrial biology in cardiac myocytes and dynamic mitochondrial biology in ne

58 Further experimentation with isolated adult cardiac myocytes and fibroblasts from double-knockout im

59 axis mediates fibrotic responses commonly in cardiac myocytes and fibroblasts induced by physico-chem

60 w, we summarize mechanoregulated pathways in cardiac myocytes and fibroblasts that lead to altered ge

61 We used isolated adult mouse cardiac myocytes and fibroblasts, as well as preclinical

62 Using membranes prepared from adult rat cardiac myocytes and fibroblasts, we found that MMP14 ac

63 agnitude and translocation of ERK1/2 between cardiac myocytes and fibroblasts.

64 the functional role of Golgi betaARs in rat cardiac myocytes and found they activate Golgi localized

65 gical processes such as spontaneous beats in cardiac myocytes and glucose-dependent ATP increase in p

66 asm and the mitochondrial matrix of isolated cardiac myocytes and in Langendorff-perfused hearts base

67 d and used to determine the EGSH in isolated cardiac myocytes and in Langendorff-perfused hearts.

68 n ER stress, ERAD, and viability in cultured cardiac myocytes and in the mouse heart, in vivo.

69 lial cells and vascular smooth muscle cells, cardiac myocytes and inflammatory cells, like monocyte/m

70 ransitions in isolated murine and guinea pig cardiac myocytes and mitochondria.

71 ss response on ischemia/reperfusion (I/R) in cardiac myocytes and mouse hearts.

72 emonstrating concomitant isolation of viable cardiac myocytes and nonmyocytes from the same adult mou

73 ution microscopy, we demonstrate that in rat cardiac myocytes and other cell types mitochondrial PDE2

74 at miR-29 promotes pathologic hypertrophy of cardiac myocytes and overall cardiac dysfunction.

75 mic globular hemoprotein highly expressed in cardiac myocytes and oxidative skeletal myofibers.

76 plex electrophysiology protocols from single cardiac myocytes and then used to tune model parameters

77 flow and delivery of nutrients to the local cardiac myocytes and to augment ATP production by their

78 action potential conduction, contraction of cardiac myocytes, and actin filament-based movement of c

79 ched in the adipocytes, smooth muscle cells, cardiac myocytes, and immune cells.

80 cilia and the intercalated disks of isolated cardiac myocytes, and performed targeted patch-clamp rec

81 (2)AR) signals through both G(s) and G(i) in cardiac myocytes, and the G(i) pathway counteracts the G

82 oplasmic reticulum (SR) Ca release events in cardiac myocytes, and they have a typical duration of 20

83 e cardiac collagen volume fraction (CVF) and cardiac myocyte apoptosis index in aFGF-NP+UTMD group re

84 s group showed similar results (MCD, CVF and cardiac myocyte apoptosis index) to other aFGF treatment

85 free mitochondrial calcium concentration in cardiac myocytes are largely unknown.

86 Changes in redox potentials of cardiac myocytes are linked to several cardiovascular di

87 Near term fetal cardiac myocytes are more sensitive than younger myocyte

88 ellular calcium (Ca(2+)) cycling dynamics in cardiac myocytes are spatiotemporally generated by stoch

89 ch contraction and haemodynamic disturbance, cardiac myocytes are subjected to fluid shear stress as

90 larized mitochondria in resting neonatal rat cardiac myocytes, as well as in those treated with TNF o

91 arizing current passed by Kv11.1 channels in cardiac myocytes, as well as the current passed in respo

92 Development of myocardial fibrosis, cardiac myocyte atrophy and loss of sarcomeric proteins

93 was studied in LV muscle strips and isolated cardiac myocytes before and after elimination of titin-b

94 eatment protects cultured neonatal and adult cardiac myocytes, but not Mfn1 knockout cells, from stre

95 g transcription factor 6alpha (ATF6alpha) in cardiac myocytes, but the roles of ATF6alpha or the rela

96 , nNOS is the most relevant source for NO in cardiac myocytes, but this nNOS is not located in mitoch

97 nd that amylin deposition negatively affects cardiac myocytes by inducing sarcolemmal injury, generat

98 We followed changes in cardiac myocyte Ca(2+) and Na(+) regulation from the for

99 In cardiac myocytes Ca(2+) is a crucial regulator of contra

100 cell types within the myocardium, including cardiac myocytes, cardiac fibroblasts and vascular smoot

101 could find no evidence to support a burst of cardiac myocyte cell cycle activity at postnatal day 15.

102 n T-Cre;CyclinA2-LacZ-EGFP mice, we examined cardiac myocyte cell cycle activity during embryogenesis

103 Discerning cardiac myocyte cell cycle behavior is challenging owing

104 tanding of the molecular circuitry governing cardiac myocyte cell cycle regulation is required.

105 -specific cell cycle reporter for studies of cardiac myocyte cell cycle regulation.

106 While cardiac myocyte cell diameter regressed to the level of

107 ifferent cAMP pools have opposing effects on cardiac myocyte cell size.

108 heart; however, the endogenous structure of cardiac myocyte chromatin has never been determined.

109 In cardiac myocytes, clusters of type-2 ryanodine receptors

110 The function of ZO-1 in cardiac myocytes (CM) is largely unknown.

111 mechanical signals in many cells, including cardiac myocytes (CM).

112 In the beating heart, cardiac myocytes (CMs) contract in a coordinated fashion

113 RATIONALE: During each beat, cardiac myocytes (CMs) generate the mechanical output ne

114 art require strong and stable connections of cardiac myocytes (CMs) with the extracellular matrix (EC

115 LADs encompass ~20% of the genome in human cardiac myocytes comprised several hundred coding and no

116 While cardiac myocytes contain several isoforms of NO synthase

117 gulates actin-myosin interaction and thereby cardiac myocyte contraction and relaxation.

118 Cardiac myocyte contraction is caused by Ca(2+) binding

119 as accompanied by increased cell cohesion in cardiac myocyte cultures and murine heart slices.

120 3A (PDE3A) gene encodes a PDE that regulates cardiac myocyte cyclic adenosine monophosphate (cAMP) le

121 human-induced pluripotent stem cell-derived cardiac myocytes deficient in SCN5A.

122 actor-kappaB signaling was also activated in cardiac myocytes derived from a patient with ACM.

123 ed the capabilities of our device to support cardiac myocytes derived from human induced pluripotent

124 um release activity (n=14, P<0.013) in human cardiac myocytes derived from induced pluripotent stem c

125 ling hMSCs were cocultured with normal human cardiac myocytes derived from induced pluripotent stem c

126 ling hMSCs prevented Ca2+ alternans in human cardiac myocytes derived from induced pluripotent stem c

127 pontaneous calcium release activity in human cardiac myocytes derived from induced pluripotent stem c

128 ed novel pathways regulated by TBX5 in human cardiac myocyte development.

129 y, we modeled the anatomical structures in a cardiac myocyte diad, to predict the effects of anatomic

130 TAC hearts revealed significantly increased cardiac myocyte diameter and mild fibrosis.

131 mal mouse hearts, but were upregulated after cardiac myocyte-directed Drp1 gene deletion in adult mic

132 s, indicating that the function of miR-29 in cardiac myocytes dominates over that in non-myocyte cell

133 and membrane potential (DeltaPsim) in adult cardiac myocytes during cyclic sarcoplasmic reticulum Ca

134 rriers to diffusion that are expected in the cardiac myocyte dyadic space, cAMP compartmentation did

135 mediated by a reduction in the expression of cardiac myocyte enhancer factor 2a.

136 Our data demonstrated that right ventricular cardiac myocytes exhibited reduced cell cycle activity r

137 ) and DNA sequencing were performed in adult cardiac myocytes following development of pressure overl

138 ntially expressed with beta2 in T-tubules of cardiac myocytes, forming alpha2beta2 heterodimers.

139 n cardiac myocytes from wild-type but not in cardiac myocytes from ATF6 knockout mice.

140 At the cellular level, adult cardiac myocytes from Dusp8 gene-deleted mice were thick

141 ural and functional investigation of SOCE in cardiac myocytes from healthy mice (wild type; WT) and f

142 Single adult cardiac myocytes from mice treated with AAV9-M7.8L showe

143 le-cell and single-nucleus transcriptomes of cardiac myocytes from murine HF models and human patient

144 ng in ACM models in vitro and in vivo and in cardiac myocytes from patient induced pluripotent stem c

145 e in the field focusing on the withdrawal of cardiac myocytes from the cell cycle during the transiti

146 ADP-AM failed to enhance Ca(2+) responses in cardiac myocytes from Tpcn2(-/-) mice, unlike myocytes f

147 ical ER stressor, tunicamycin, and by I/R in cardiac myocytes from wild-type but not in cardiac myocy

148 nol-induced increase in Ca(2+) transients in cardiac myocytes from WT but not CD38(-/-) mice.

149 her important signalling enzymes determining cardiac myocyte function and phenotype.

150 a(2+) concentration regulate many aspects of cardiac myocyte function.

151 al analyses revealed interactions within the cardiac myocyte genome at 5-kb resolution, enabling exam

152 ng and ER proteostasis are challenged during cardiac myocyte growth.

153 We unexpectedly found that cardiac myocyte GSK-3 is essential for cardiac homeostas

154 Together, our findings suggest that cardiac myocyte GSK-3 is required to maintain normal car

155 space with restricted diffusion for Na(+) in cardiac myocytes has been inferred from a transient peak

156 Stretching single ventricular cardiac myocytes has been shown experimentally to activa

157 adult hearts containing mostly post-mitotic cardiac myocytes have lost this ability.

158 irectly to test this is problematic, because cardiac myocytes have many Gq-coupled receptors.

159 Cardiac myocytes have multiple cell autonomous mechanism

160 nary artery smooth muscle cells (HCASMC) and cardiac myocytes (HCM), leading to upregulation of antio

161 human induced pluripotent stem cell-derived cardiac myocytes (hiPSC-CM) demonstrated that ERRgamma a

162 hers' expression as well as transcription in cardiac myocytes; however, only Hmgb2 does so in a manne

163 t of specific inhibition of selected PDEs on cardiac myocyte hypertrophic growth.

164 rse aortic constriction and exercise-induced cardiac myocyte hypertrophy and impaired cardiac functio

165 hosphatase calcineurin is a key regulator of cardiac myocyte hypertrophy in disease.

166 ZBTB17 also regulated cardiac myocyte hypertrophy in vitro and in vivo in a ca

167 We report that asymmetrical cardiac myocyte hypertrophy is modulated by SRF (serum r

168 eel exercise, both of which promote adaptive cardiac myocyte hypertrophy with preserved cardiac funct

169 olgi resident beta1ARs prevents NE dependent cardiac myocyte hypertrophy.

170 thm telemetry, optical mapping, and isolated cardiac myocyte imaging were used to quantify arrhythmia

171 characterized by asymmetrical growth of the cardiac myocyte in mainly width or length, respectively.

172 thesized that similar effects would occur in cardiac myocytes in a lipophilicity-dependent manner bet

173 DCM, Tp53 gene was conditionally deleted in cardiac myocytes in mice expressing the LMNA(D300N) prot

174 iRNAs in vivo develop into mature functional cardiac myocytes in situ, and whether reprogramming lead

175 cycle activity relative to left ventricular cardiac myocytes in the immediate perinatal period.

176 n, we modeled the Holt-Oram syndrome in iPSC-cardiac myocytes in vitro and uncovered novel pathways r

177 Targeted deletion of miR-29 in cardiac myocytes in vivo also prevents cardiac hypertrop

178 that CASK localizes at lateral membranes of cardiac myocytes, in association with dystrophin.

179 ted by processes that extend well beyond the cardiac myocyte, including important roles for pericardi

180 earts, supporting long-term reprogramming of cardiac myocytes induced by hypoxia during critical peri

181 NCA treatment of cardiac myocytes induced translocation of PKA and phosph

182 s, uncover a novel contributing mechanism to cardiac myocyte injury in type 2 diabetes, and suggest a

183 fibroblasts from double-knockout implicated cardiac myocytes intrinsic factors responsible for obser

184 The ultrastructure of the cardiac myocyte is remarkable for the high density of mi

185 efractoriness of calcium (Ca(2+)) release in cardiac myocytes is an important factor in determining w

186 About 99% of the cytoplasmic calcium in cardiac myocytes is bound to buffers, and their properti

187 Gq signaling in cardiac myocytes is classically considered toxic.

188 ably, dynamic CpG and non-CpG methylation in cardiac myocytes is confined to A compartments.

189 achieving gene expression in the majority of cardiac myocytes is essential.

190 )plasmic reticulum calcium ATPase (SERCA) in cardiac myocytes is modulated by an inhibitory interacti

191 parts of the calcium signalling apparatus in cardiac myocytes is unknown.

192 le NO synthases (NOSs) are also expressed in cardiac myocytes, it is unclear whether they control res

193 Cardiac myocyte KLF5 is a transcriptional regulator of P

194 een attributed to perturbed Ca2+ handling in cardiac myocytes leading to spontaneous Ca2+ release and

195 Induction of O2 (-) production in H9C2 cardiac myocytes led to the release of a transferable fa

196 orter, whereas DUSP8 overexpression promoted cardiac myocyte lengthening with a loss of thickness.

197 At the cardiac myocyte level, colon ascendens stent peritonitis

198 correlated with higher expression of mature cardiac myocyte markers.

199 RRalpha and gamma are critical regulators of cardiac myocyte maturation, serving as transcriptional a

200 dings demonstrate the pivotal roles of local cardiac myocyte metabolism and K(ATP) channels and the m

201 Mechanistically, we found cardiac myocyte miR-29 to de-repress Wnt signaling by di

202 e show that ATM is found endogenously within cardiac myocyte mitochondria under normoxic conditions a

203 ce with established cardiomyopathy, restored cardiac myocyte mitochondrial membrane potential and fla

204 Cardiac myocyte mitochondrial metabolic activity was ass

205 Cardiac myocyte model systems have been developed to stu

206 rogram responsible for modulating changes in cardiac myocyte morphology that occur secondary to patho

207 ngestive heart failure typically arises from cardiac myocyte necrosis/apoptosis, associated with the

208 Cardiac myocytes normally initiate action potentials in

209 Cardiac myocyte nuclear and cellular RNA expression prof

210 The aim was to purify cardiac myocyte nuclei from hearts of different species

211 High sorting purity was confirmed for cardiac myocyte nuclei isolated from mice, rats, and hum

212 cardiac tissue samples were used to isolate cardiac myocyte nuclei.

213 Here, we report that cardiac myocytes of heterozygous mice carrying a catecho

214 ing a maximal +34-mV shift in neonatal mouse cardiac myocytes or Chinese hamster ovary (CHO) cells ex

215 ar concordant or discordant Ca2+alternans in cardiac myocytes or spatially concordant or discordant C

216 unit KChIP2, which regulates Kv4 channels in cardiac myocytes, partially relieved Kv4.3 but not Kv4.2

217 Cardiac myocyte passive tension was significantly increa

218 A with selective inhibitor TP-10, attenuated cardiac myocyte pathological hypertrophy induced by Angi

219 We report enhanced cardiac myocyte performance by acute titration of cardia

220 hrine, and isoproterenol, but did not affect cardiac myocyte physiological hypertrophy induced by IGF

221 To (re)initiate cardiac myocyte proliferation in adult mammalian hearts,

222 an amphibians leading to the hypothesis that cardiac myocyte proliferation is a major driver of heart

223 function after cardiac damage, induction of cardiac myocyte proliferation is an attractive therapeut

224 ors and the thiol-oxidizing agent diamide on cardiac myocyte protein phosphorylation and oxidation.

225 data suggest that the NCA-mediated effect on cardiac myocyte protein phosphorylation orchestrates alt

226 onatal mouse hearts containing proliferating cardiac myocytes regenerate even extensive injuries, whe

227 containing ubiquitin-tagged proteins within cardiac myocytes related to proteasome dysfunction and i

228 f DNA methylation in embryonic stem cells or cardiac myocytes, respectively, does not alter genome-wi

229 We generated transgenic mice with cardiac myocyte-restricted expression of Grx1-roGFP2 tar

230 Mechanistically, loss of GSK-3 in adult cardiac myocytes resulted in induction of mitotic catast

231 mtDNA damage in cardiac myocytes resulting from increased oxidative stre

232 In vitro REEP5 depletion in mouse cardiac myocytes results in SR/ER membrane destabilizati

233 diac myocyte translatome by purifying tagged cardiac myocyte ribosomes from cardiac lysates and subje

234 In a cardiac myocyte, RyRs group into clusters of variable si

235 How does the cardiac myocyte sense changes in preload or afterload?

236 2+) spark initiation after Ca(2+) release in cardiac myocytes should inhibit further Ca(2+) release d

237 Double-knockout cardiac myocytes showed cell cycle progression resulting

238 erged de novo into terminally differentiated cardiac myocytes, smooth muscle and vascular endothelial

239 These effects were lost upon cardiac myocyte-specific Atf6 deletion in the heart, dem

240 Our data highlight advantages of a cardiac myocyte-specific cell cycle reporter for studies

241 Cardiac myocyte-specific CIP4 gene deletion in mice atte

242 Cardiac myocyte-specific deletion of Atf6 (ATF6 cKO [con

243 Cardiac myocyte-specific expression of LMNA(D300N), asso

244 ctor, in the lethal cardiomyopathy evoked by cardiac myocyte-specific interruption of dynamin-related

245 iPLA2gamma in cardiac myocytes, we generated cardiac myocyte-specific iPLA2gamma knock-out (CMiPLA2ga

246 iPLA2gamma, germ-line iPLA2gamma(-/-) mice, cardiac myocyte-specific iPLA2gamma transgenic mice, and

247 We generated cardiac myocyte-specific Klf5 knockout mice that showed

248 xpression profiles and epigenetic marks in a cardiac myocyte-specific manner.

249 We generated tamoxifen-inducible cardiac myocyte-specific mice lacking both GSK-3 isoform

250 A novel cardiac myocyte-specific Speg conditional knockout (MCM-

251 ated to defects of subcellular components in cardiac myocytes, specifically in the dyadic cleft, whic

252 We conclude that titin-based cardiac myocyte stiffening acutely after MI is partly me

253 METHODS AND Knockdown of ATF6 in cardiac myocytes subjected to I/R increased reactive oxy

254 Knockdown of ATF6 in cardiac myocytes subjected to I/R increased reactive oxy

255 into our previous local-control model of the cardiac myocyte that describes excitation-contraction co

256 e uniquely-adapted membrane invaginations in cardiac myocytes that facilitate the synchronous release

257 nal-regulated kinases 1/2 signaling in adult cardiac myocytes that then alters the length-width growt

258 In cardiac myocytes, the activation of inner membrane pores

259 of the sarcomere, the structural unit of the cardiac myocytes, the Frank-Starling mechanism consists

260 mtDNA repair machinery has been described in cardiac myocytes, the regulation of this repair has been

261 In wild-type cardiac myocytes, the selective alpha-1A agonist A61603-

262 In cardiac myocytes, there are several Ca(2+) -sensitive po

263 lays a central role in Ca(2+) homeostasis in cardiac myocytes through regulation of the sarco(endo)pl

264 Notch activation reprograms cardiac myocytes to an induced Purkinje-like state chara

265 tective effects of RF-RDN acting directly on cardiac myocytes to attenuate cell death and protect aga

266 Using permeabilized cardiac myocytes to eliminate any contribution of plasma

267 sor anchored onto the myofilaments in rabbit cardiac myocytes to examine PKA activity at the myofilam

268 This work provides structural evidence in cardiac myocytes to indicate the formation of microdomai

269 STIM1 can associate with Orai in cardiac myocytes to produce a Ca(2+) influx pathway that

270 on is closely associated with the ability of cardiac myocytes to proliferate.

271 m of AC, commonly recognized as a disease of cardiac myocytes, to include nonmyocyte cells in the hea

272 After pressure overload, we monitored the cardiac myocyte translatome by purifying tagged cardiac

273 d sarcomere strain were also imaged in paced cardiac myocytes under mechanical load, revealing sponta

274 itochondrial permeability transition pore in cardiac myocytes under stress.

275 Spontaneous calcium (Ca) waves in cardiac myocytes underlie delayed afterdepolarizations (

276 (2+) spark (LCS) activity in intact isolated cardiac myocytes using fast confocal line scanning with

277 In ventricular cardiac myocytes (VCM), Gbeta5 deficiency provided subst

278 a phosphaturic hormone that directly targets cardiac myocytes via FGF receptor (FGFR) 4 thereby induc

279 ump activity regulate internal Ca release in cardiac myocytes via Na/Ca exchange.

280 st that CO induces arrhythmias in guinea pig cardiac myocytes via the ONOO(-)-mediated inhibition of

281 cal in inhibiting mitochondrial function and cardiac myocyte viability using SAMbetaA, a rationally-d

282 Expression of miR-184 in the heart and cardiac myocyte was developmentally downregulated and wa

283 The number of EdU(+) cardiac myocytes was increased in CBSC- versus vehicle-

284 T2 p.R173W) in patient-specific iPSC-derived cardiac myocytes, we demonstrated that the knockout stra

285 ifically identify the roles of iPLA2gamma in cardiac myocytes, we generated cardiac myocyte-specific

286 tion or the patch-clamp technique in beating cardiac myocytes, we identified a neuronal NO synthase (

287 r determine the impact of hyperamylinemia on cardiac myocytes, we investigated human myocardium, comp

288 ial fission was conditionally interrupted in cardiac myocytes, we propose several new concepts that m

289 armacological inhibition of iNOS in isolated cardiac myocytes, we reveal that an increase of expressi

290 Cardiac myocytes were isolated with yields comparable to

291 Freshly isolated cardiac myocytes were loaded with the Ca(2+)-indicator f

292 Cultured cardiac myocytes were subjected to different stresses in

293 Cardiac myocytes were the most commonly used cell type (

294 ), was delivered into acutely isolated mouse cardiac myocytes, where either one- and two-photon uncag

295 e length-width growth dynamics of individual cardiac myocytes, which further alters contractility, ve

296 catalase gene and were shown to bind ATF6 in cardiac myocytes, which increased catalase promoter acti

297 epresent a subcellular sarcomeric space in a cardiac myocyte with varying detail.

298 Treatment of cardiac myocytes with CTRP9 protein led to suppression o

299 Stimulation of the cardiac myocytes with isoprenaline, angiotensin II, or e

300 Membrane permeabilization of cardiac myocytes with saponin and/or Triton X-100 increa