ライフサイエンスコーパス: cardiomyocyte

1 mesoderm), JUN and FOS families, and MEIS2 (cardiomyocyte).

2 teractions with the microvasculature and the cardiomyocyte.

3 two levels of resting membrane potential in cardiomyocytes.

4 cardiomyoblasts, neuronal cells, and primary cardiomyocytes.

5 tk expression in platelets, T lymphocytes or cardiomyocytes.

6 an heart's low inherent capacity to form new cardiomyocytes.

7 art, isolated tissue preparations and single cardiomyocytes.

8 view has been that metoprolol acts mainly on cardiomyocytes.

9 -knockout mice and Herpud1 siRNA-treated rat cardiomyocytes.

10 free mitochondrial calcium concentration in cardiomyocytes.

11 s, but not genomic RNAs, in human and murine cardiomyocytes.

12 BIN1-microfolds are externally released from cardiomyocytes.

13 phenotype results from the loss of GAS2L3 in cardiomyocytes.

14 gulator FoxO in the nuclei of ncx1-deficient cardiomyocytes.

15 notably muscle creation through division of cardiomyocytes.

16 connected in vitro neonatal rat ventricular cardiomyocytes.

17 /-) mice because of changes in subepicardial cardiomyocytes.

18 ain the normal resting membrane potential of cardiomyocytes.

19 formation and fusion activity in ventricular cardiomyocytes.

20 induce cytokine response in macrophages and cardiomyocytes.

21 urther establish that TNFalpha induces IR in cardiomyocytes.

22 on protein quality control and autophagy in cardiomyocytes.

23 tion into fibroblast-like cells but not into cardiomyocytes.

24 that govern the contractile function of the cardiomyocytes.

25 y maintain the resting membrane potential of cardiomyocytes.

26 ction impairment and myofibril disruption in cardiomyocytes.

27 e potential and depolarize in synchrony with cardiomyocytes.

28 evels of resting membrane potential of human cardiomyocytes.

29 oning by a mechanism stemming primarily from cardiomyocytes.

30 osyltransferase and stimulates glycolysis in cardiomyocytes.

31 eceptors, which was blunted in Nod1(-/-)-PMI cardiomyocytes.

32 S. pneumoniae rapidly adhered to and invaded cardiomyocytes.

33 soderm, cardiac mesoderm, and differentiated cardiomyocytes.

34 mammalian heart undergoes limited renewal of cardiomyocytes.

35 dult and human pluripotent stem cell-derived cardiomyocytes; (2) 2-dimensional in vitro models, such

36 sters of human pluripotent stem cell-derived cardiomyocytes; (3) 3-dimensional multicellular in vitro

37 cent endoderm control the medial movement of cardiomyocytes, a process referred to as cardiac fusion.

38 GAS2L3 results in premature binucleation of cardiomyocytes accompanied by unresolved midbody structu

39 nous IFN-alpha did not substantially protect cardiomyocytes against CVB3.

40 IONALE: There are several methods to measure cardiomyocyte and muscle contraction, but these require

41 Profiling of cardiomyocyte and nonmyocyte transcriptional programs un

42 o mesodermal, cardiac progenitors and mature cardiomyocytes and an enhanced ability to differentiate

43 nflammasome and caspase-I hyperactivation in cardiomyocytes and cardiac macrophages in peri-infarct r

44 cell-derived factor 1, that is expressed in cardiomyocytes and decreases calcium influx across the L

45 mon platform for directed differentiation of cardiomyocytes and endothelial subtypes from hPSCs.

46 ic and induced pluripotent stem cell-derived cardiomyocytes and fibroblasts with organotypic function

47 or populations that enable the derivation of cardiomyocytes and functionally distinct endothelial cel

48 sa-miR-590-3p both in primary neonatal mouse cardiomyocytes and in vivo.

49 heart, Smad3 signaling is activated in both cardiomyocytes and interstitial cells.

50 ncer patients, elevate glucose and sensitize cardiomyocytes and mice to the cancer drug doxorubicin (

51 and electrophysiological properties of both cardiomyocytes and neurons.

52 exogenous mitochondria in human iPS-derived cardiomyocytes and primary cardiac fibroblasts.

53 In cardiomyocytes and smooth muscle cells, cyclic AMP (cAMP

54 sing directions across the S(E)R membrane in cardiomyocytes and that changes in their activity play a

55 es PDK4 (pyruvate dehydrogenase kinase 4) in cardiomyocytes and that elevated PDK4 levels in late pre

56 MitoCam) was expressed in cultured adult rat cardiomyocytes and the free mitochondrial calcium concen

57 mically controls PABPC1 protein synthesis in cardiomyocytes and thereby titrates cellular translation

58 Centrifugation removes large cardiomyocytes and tissue debris producing a single cell

59 ffects by activating its nuclear receptor in cardiomyocytes and vascular endothelial cells and by reg

60 Ca(2+)-dependent transcriptional pathways in cardiomyocytes, and (3) discuss implications of excitati

61 ited inflammasome activation in macrophages, cardiomyocytes, and cardiac fibroblasts via proteinase-a

62 zithromycin in vivo and in vitro using mice, cardiomyocytes, and human ion channels heterologously ex

63 occurs via the proliferation of pre-existing cardiomyocytes, and is regulated by aerobic-respiration-

64 ttenuated cardiomyocyte hypertrophy, reduced cardiomyocyte apoptosis, fibrosis, calcium/calmodulin-de

65 erations in cardiac morphology, and elevated cardiomyocyte apoptosis, which were mitigated in the cat

66 y with improved cardiac function and reduced cardiomyocyte apoptosis.

67 rdial ischaemia-reperfusion-injury (IRI) and cardiomyocytes are a known source of complement proteins

68 human induced pluripotent stem cell-derived cardiomyocytes are a powerful model for screening varian

69 HLHS-iPSC-derived cardiomyocytes are characterised by a lower beating rate

70 Cardiomyocytes are organized in microstructures termed s

71 an pluripotent stem-cell-derived ventricular cardiomyocytes are strategically aligned to reproduce ke

72 abinoid signaling, glucose uptake, and IR in cardiomyocytes are understudied.

73 lso shown a change in DNA methylation within cardiomyocytes as a result of in utero exposure to diese

74 neage tracing to mark the Nppa(+) or Hey2(+) cardiomyocytes as trabecular and compact components of t

75 atrium and ventricle appeared to be working cardiomyocytes based on their morphological appearance a

76 Characterization of cardiomyocyte beat patterns is needed for quality contro

77 cation even during vigorous activity such as cardiomyocyte beating.

78 imarily because of proliferation of existing cardiomyocytes but not from the differentiation of putat

79 Red and photoactivable mtPA-GFP, in isolated cardiomyocytes by confocal microscopy.

80 crease of expression and activity of iNOS in cardiomyocytes by VCP is an essential mechanistic link o

81 In cardiomyocytes, Ca(2+) is the central element of excitat

82 ecting cardiomyocyte membrane potentials and cardiomyocyte-cardiomyocyte gap junctional coupling, TGF

83 Conversely, in the homocysteine-treated cardiomyocytes, CBS and miR-133a were downregulated and

84 dicating that the majority of injury-induced cardiomyocyte cell cycle activity results in binucleatio

85 ions between pathways that are important for cardiomyocyte cell cycle reentry, with relevance to vent

86 nd regeneration, the mechanisms that promote cardiomyocyte cell cycle remain incompletely understood.

87 o mechanisms by which NUMB and NUMBL promote cardiomyocyte cell cycle withdrawal and highlight previo

88 en our particular datasets on cultured human cardiomyocyte cell lines, we find that, while convention

89 onally, in human embryonic stem cell-derived cardiomyocytes challenged with TNFalpha or FFA, we demon

90 alian vertebrates such as zebrafish activate cardiomyocyte (CM) division after tissue damage to regen

91 C5a interacts with its receptors on cardiomyocytes (CMs), resulting in redox imbalance and c

92 ncentrations reduced insulin sensitivity and cardiomyocyte contractility, which was rescued by CD36 s

93 p junctional coupling, TGF-beta1 depolarized cardiomyocytes coupled to myofibroblasts by approximatel

94 asts and by cessation of ectopic activity of cardiomyocytes coupled to myofibroblasts during pharmaco

95 Cardiomyocyte creation by human pluripotent stem cells (

96 We also used a neonatal rat cardiomyocyte culture system to elucidate the mechanisms

97 abeled induced pluripotent stem cell-derived cardiomyocyte cultures.

98 In isolated wild-type cardiomyocytes, Cx43 protein content decreased on myelop

99 tile dysfunction, cardiomyocyte hypertrophy, cardiomyocyte death, and N-terminal pro B-type natriuret

100 Of note, SRC-2 knockdown in cardiomyocytes decreased VEGF expression and secretion t

101 TGF-beta1-dependent cardiomyocyte depolarization resulted from electrotonic

102 mRNA sequences analyzed from a population of cardiomyocytes derived from human induced pluripotent st

103 In the present study, we show that human cardiomyocytes derived from induced pluripotent stem cel

104 Under hypokalaemic conditions, both human cardiomyocytes derived from induced pluripotent stem cel

105 Similarly, primary cardiomyocytes derived from XLalphas knockout (XLKO) pup

106 odulatory role in fine-tuning human-specific cardiomyocyte development by forming a regulatory networ

107 Heart Brake LncRNA 1 (HBL1), which regulates cardiomyocyte development from human induced pluripotent

108 differentiation of HLHS-iPSC restored their cardiomyocyte differentiation capacity and beating rate

109 n accessibility at genome-wide levels during cardiomyocyte differentiation derived from 2 hiPSC lines

110 d to decreased HBL1 expression and increased cardiomyocyte differentiation efficiency.

111 as knockdown and knockout of HBL1 increased, cardiomyocyte differentiation from hiPSCs.

112 s (ie, from mesoderm to cardiac mesoderm) of cardiomyocyte differentiation remains limited.

113 is revealed that transcriptomes during early cardiomyocyte differentiation were highly concordant bet

114 y important roles at different stages during cardiomyocyte differentiation, such as T and eomesodermi

115 strongly correlated with different stages of cardiomyocyte differentiation.

116 Cardiomyocyte-directed expression of the inhibitory CREM

117 erived induced pluripotent stem cell-derived cardiomyocytes display (1) significantly prolonged actio

118 These cardiomyocytes display N-shaped current-voltage relation

119 7) (which accumulates in doxorubicin-treated cardiomyocytes) displays decreased C-terminal tail primi

120 an important source of oxygen to sustain the cardiomyocyte during extended ischemia.

121 ing the transcriptional program of postnatal cardiomyocytes during heart development has been shown,

122 We conclude that NS-cardiomyopathy involves cardiomyocytes, ECs and fibroblasts, TNF/IL6 signalling

123 s demonstrated by immediate normalization of cardiomyocyte electrophysiology after targeted disruptio

124 y co-culturing human primary or iPSC-derived cardiomyocytes, endothelial cells and fibroblasts at rat

125 h as exosomes secreted from the iPSC-derived cardiomyocytes exert protective effects by transferring

126 Human cardiomyocytes exhibit two levels of resting membrane po

127 The viability of cardiomyocytes exposed to Eta2Omicron2 was reduced and d

128 or pharmacological inhibition of v-ATPase in cardiomyocytes exposed to low palmitate concentrations r

129 re with preserved ejection fraction (HFpEF), cardiomyocyte-extracellular matrix interactions from exc

130 In contrast, cardiomyocytes failed to reactivate the neonatal prolife

131 [Ca(2+) ]i transient in cardiomyocytes followed similar pattern.

132 induced pluripotent stem cell (iPSC)-derived cardiomyocytes from a patient with a gain-of-function mu

133 vances have improved our ability to generate cardiomyocytes from human induced pluripotent stem cells

134 We generated iPSC-derived cardiomyocytes from patients presenting in vivo with ext

135 le cellular differentiation, specifically in cardiomyocytes from physiologically and pathologically h

136 eric z-disc also represents a nodal point in cardiomyocyte function and signaling.

137 ment catestatin (CST) may directly influence cardiomyocyte function.

138 nctional coupling between myofibroblasts and cardiomyocytes >5-fold as reflected by elevated connexin

139 ptional activities in cultured embryonic rat cardiomyocytes (H9c2).

140 f MEF2 isoform-specific function in neonatal cardiomyocytes has yielded insight into an unexpected tr

141 Endogenous cardiomyocytes have regenerative capacity at birth but t

142 METHODS AND Extending our previous hMSC-cardiomyocyte HC computational model, we incorporated ex

143 Human-induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CM) are increasingly being used fo

144 Human induced pluripotent stem cell derived cardiomyocytes (hiPSC-CMs) offer a novel in vitro platfo

145 human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) provide new possibilities for

146 human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs), but D-ala,RP produgs, includ

147 human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs), Tbx20 enhanced human KCNH2 g

148 in defining the transcriptional program for cardiomyocyte homeostasis and cardiac hypertrophy.

149 of an array of regulatory genes involved in cardiomyocyte homeostasis and disease compensation.

150 onstrate that H-Ras, but not K-Ras, promotes cardiomyocyte hypertrophy both in vivo and in vitro.

151 bition of cardiomyocyte proliferation and to cardiomyocyte hypertrophy during embryonic development.

152 Moreover, cardiomyocyte hypertrophy is blunted with cardiac fibrob

153 roved microvascular formation and attenuated cardiomyocyte hypertrophy).

154 cts of cardiac remodeling, such as fibrosis, cardiomyocyte hypertrophy, and calcium handling (Col1a2,

155 amine toxicity with contractile dysfunction, cardiomyocyte hypertrophy, cardiomyocyte death, and N-te

156 llowing TAC, cyclin D2 expression attenuated cardiomyocyte hypertrophy, reduced cardiomyocyte apoptos

157 th subsequent organ growth occurring through cardiomyocyte hypertrophy.

158 lates miR-133a that targets SP1 and inhibits cardiomyocytes hypertrophy.

159 n isoform shift, and contractile behavior of cardiomyocytes in heart tissue of PPCM and DCM patients

160 e behaviour in single membrane-permeabilized cardiomyocytes in human left ventricular heart tissue.

161 as a nearly 2-fold increase in the number of cardiomyocytes in mitosis indicating that the majority o

162 n of the human pluripotent stem cell-derived cardiomyocytes in our system recapitulates in vivo devel

163 orchestrates critical epigenetic changes in cardiomyocytes in physiological and pathological conditi

164 L5 on the electrophysiological properties of cardiomyocytes in relation to the lectin-like oxidized L

165 Tian et al. show that cardiomyocytes in the fetal compact layer also contribut

166 ntribution of c-Kit(+) cardiac stem cells to cardiomyocytes in the heart and the contribution of Sox9

167 sts capable of differentiation into striated cardiomyocytes in vitro.

168 examine the physiologic role of p53 in adult cardiomyocytes in vivo, Cre-loxP-mediated conditional ge

169 neonatal Nkx2.5+ cardiomyoblasts mature into cardiomyocytes in vivo.

170 iac gene expression and differentiation into cardiomyocytes; in contrast, restricting Hdac3 to the nu

171 In addition, alterations of the atrial cardiomyocytes, increase of noncollagen deposits in the

172 Overexpression of NDPK-C in cardiomyocytes increased cAMP levels and sensitized card

173 Overexpression of FoxO in wild type cardiomyocytes induced murf1 expression and caused myofi

174 d that 1) paracrine signaling from stretched cardiomyocytes induces CFB proliferation under mechanica

175 ial direct reprogramming of mesoderm-derived cardiomyocytes into neurons is feasible, generating cell

176 The proliferation arrest of cardiomyocytes is accompanied by binucleation through in

177 Specification of cardiomyocytes is associated with reorganization of peri

178 dy functional and bioenergetic parameters in cardiomyocytes isolated after 24-hour sepsis.

179 Single-cell recordings of cardiomyocytes isolated from HFpEF rats confirmed a dela

180 se-derived H2O2 production were required for cardiomyocyte killing.

181 by structural remodelling of the specialised cardiomyocytes known collectively as the cardiac conduct

182 experimentally calibrated hMSC PS effects on cardiomyocyte L-type calcium channel/sarcoendoplasmic re

183 usly generated directly reprogrammed induced cardiomyocyte-like cells (iCMs) by overexpression of Gat

184 gramming of cardiac fibroblasts into induced cardiomyocyte-like cells in situ represents a promising

185 ion of human dermal fibroblasts into induced cardiomyocyte-like cells via transcription factor overex

186 (GMT), can convert fibroblasts into induced cardiomyocyte-like cells, albeit with low efficiency in

187 Mammalian cardiomyocytes lose the ability to proliferate shortly a

188 hypertrophy occurs in AC and is secondary to cardiomyocyte loss and cardiac remodeling.

189 AC pathology is characterized by cardiomyocyte loss and replacement fibrosis.

190 heart is incapable of regeneration following cardiomyocyte loss, which underpins the lasting and seve

191 We were able to predict the proportion of cardiomyocytes many days before cells manifest the diffe

192 ventricular hypertrophy driven by increased cardiomyocyte mass.

193 Whereas not affecting cardiomyocyte membrane potentials and cardiomyocyte-card

194 es made of mouse embryonic stem cell-derived cardiomyocytes (mESC-CMs).

195 ng others (eg, microvascular dysfunction and cardiomyocyte/mitochondrial dysfunction).

196 nd oxidative DNA damage, and reactivation of cardiomyocyte mitosis.

197 However, tissue cultures of cardiomyocyte monolayers currently require the use of ne

198 METHODS AND Neonatal rat atrial cardiomyocyte monolayers expressing a depolarizing light

199 dimensional in vitro models, such as beating cardiomyocyte monolayers or small clusters of human plur

200 Stem cell-derived cardiomyocytes mutated to carry the effect allele had di

201 o low-grade inflammatory infiltrates without cardiomyocyte necrosis.

202 ccumulation of unrepaired SSB is observed in cardiomyocytes of the failing heart.

203 t (Ito) in EPI but not in endocardial (ENDO) cardiomyocytes of UNx rats led to a decreased transmural

204 Raf1(L613V) expression in cardiomyocytes or activated fibroblasts exacerbates pres

205 tream of cGMP involve BK channels present in cardiomyocytes or in other cardiac cell types.

206 re phospho-histone H3+ (a marker of mitosis) cardiomyocytes (p = 0.04), and noncardiomyocytes (p = 0.

207 These Pnmt(+) cell derived cardiomyocytes (PdCMs) are similar to conventional myocy

208 tile cycles, an important characteristics of cardiomyocyte phenotype.

209 ich sustained FGF signaling acts to suppress cardiomyocyte plasticity and to preserve the integrity o

210 erexpression of Tnni3k in zebrafish promoted cardiomyocyte polyploidization and compromised heart reg

211 rentiate into vascular endothelial cells and cardiomyocytes possibly by FGF and BMP signaling, respec

212 iled by developmental mechanisms that render cardiomyocytes post-mitotic.

213 study aimed to characterize a population of cardiomyocyte precursors in the neonatal heart and to de

214 uripotent stem cells (iPSC) and iPSC-derived cardiomyocytes presents a valuable opportunity to replen

215 lted in elevated MNDCM content and increased cardiomyocyte proliferation after injury.

216 Cardiomyocyte proliferation and heart functional recover

217 ed neovascularization, neutrophil clearance, cardiomyocyte proliferation and scar resolution.

218 hat GAS2L3 deficiency leads to inhibition of cardiomyocyte proliferation and to cardiomyocyte hypertr

219 identified Cnot3 as a critical regulator in cardiomyocyte proliferation at the late stage of cardiac

220 tudy supported the model that Cnot3 enhances cardiomyocyte proliferation by promoting cell cycle inhi

221 viate oxidative DNA damage, thereby inducing cardiomyocyte proliferation in adult mammals.

222 Despite the importance of cardiomyocyte proliferation in cardiac development and r

223 to the Hippo pathway effector Yap to inhibit cardiomyocyte proliferation in mice.

224 Uncovering the molecular basis of mammalian cardiomyocyte proliferation may eventually lead to bette

225 yocardial infarction, although the degree of cardiomyocyte proliferation observed in this model sugge

226 erate their hearts after apical resection by cardiomyocyte proliferation.

227 Stem cell-derived cardiomyocytes provide a promising tool for human develo

228 combined with 3D confocal imaging of beating cardiomyocytes provides a functional 3D map of active EC

229 Overexpression of microRNA-146a in cardiomyocytes provoked cardiac hypertrophy and left ven

230 nd functional features, and drug response of cardiomyocytes (PSC-CMs) and endothelial cells (PSC-ECs)

231 In cultured H9c2 cardiomyocytes, Rac1 activation with l-buthionine sulfox

232 uingly, transgenic overexpression of GCH1 in cardiomyocytes reduces the thickness of interventricular

233 Adult mammalian cardiomyocyte regeneration after injury is thought to be

234 modulate hypertrophy and gene expression in cardiomyocytes remain unclear.

235 ractions of heart-invaded S. pneumoniae with cardiomyocytes remain unclear.

236 d functional maturation of stem cell-derived cardiomyocytes remains a key challenge for applications

237 Here, we tested the hypothesis that enhanced cardiomyocyte renewal in transgenic mice expressing cycl

238 In both of these scenarios, cardiomyocyte renewal occurs via the proliferation of pr

239 an myocardium can undergo a low level of new cardiomyocyte renewal of approximately 1% per year, whic

240 ized reparative capacity involving more than cardiomyocyte renewal.

241 Direct reprogramming of fibroblasts to cardiomyocytes represents a potential means of restoring

242 By contrast, REST overexpression in cultured cardiomyocytes represses p21 and increases proliferation

243 he pathways that can be modulated to enhance cardiomyocyte reprogramming.

244 Our goal was to determine whether cardiomyocytes respond to AC progression by pathological

245 dingly, Ca(2+)-spark analysis in isolated TG cardiomyocytes revealed remarkably reduced Ca(2+) leakag

246 RATIONALE: Postmitotic cells, such as cardiomyocytes, seem to be particularly susceptible to p

247 trations or pathological hypokalaemia, human cardiomyocytes show both hyperpolarized and depolarized

248 Cardiomyocyte size and collagen accumulation were signif

249 resolution and then seeded the scaffold with cardiomyocytes, smooth muscle cells, and endothelial cel

250 human-induced pluripotent stem cell-derived cardiomyocytes, smooth muscle cells, and endothelial cel

251 ng myocardial infarction, myofibroblast- and cardiomyocyte-specific activation of Smad3 has contrasti

252 ospho-silenced cTnIS200A, each driven by the cardiomyocyte-specific alpha-myosin heavy chain promoter

253 METHODS AND We generated cardiomyocyte-specific Cas9 mice and demonstrated that C

254 Cardiomyocyte-specific deletion of GAS2L3 confirmed that

255 iological and stress conditions, mice with a cardiomyocyte-specific deletion of PMCA1 (PMCA1(cko) ) a

256 both organ and cellular levels in mice with cardiomyocyte-specific deletion of PMCA1 (PMCA1(cko) ) T

257 ecreases sustained cardiac function, but the cardiomyocyte-specific effects of SRC-2 in these changes

258 Here, we report that cardiomyocyte-specific loss of SRC-2 (SRC-2 CKO) results

259 We define a novel cardiomyocyte-specific regulatory mechanism for TGF-beta

260 is a critical barrier for the acquisition of cardiomyocyte-specific splicing patterns in fibroblasts.

261 se a range of state-of-the-art methods and a cardiomyocyte-specific, tamoxifen-activated, PKP2 knocko

262 in decreased cell proliferation and enhanced cardiomyocyte specification.

263 High cardiomyocyte stiffness contributed to stiffness of fail

264 ctivity of protein clearance pathways in the cardiomyocyte, such as proteasomal degradation and autop

265 uld supply basic energy needs in non-beating cardiomyocytes, suggesting that increased collateral cir

266 rogenic Cl(-)/HCO3(-) exchange activities in cardiomyocytes, suggesting the potential role of Slc26a6

267 MEF2A and MEF2D were absolutely required for cardiomyocyte survival, whereas MEF2C, despite its major

268 ssion alleviated the effects of H2O2 on H9c2 cardiomyocyte survival.

269 Thus, in the cardiomyocyte, the mitochondrial Ca(2+) microdomain is w

270 Similarly, in HL-1 cardiomyocytes, the drug slowed sinus automaticity, redu

271 In ventricular cardiomyocytes, the membrane deformation protein cardiac

272 ) oscillations with a decreased frequency in cardiomyocytes through recordings of intracellular Ca(2+

273 CPVT2 and to use the generated hiPSC-derived cardiomyocytes to gain insights into patient-specific di

274 Exposure of H9c2 cardiomyocytes to H2O2 or pharmacologic inhibition of H2

275 yocytes increased cAMP levels and sensitized cardiomyocytes to isoprenaline-induced augmentation of c

276 ous cardiac c-kit(+) cells rarely contribute cardiomyocytes to the adult heart.

277 induced pluripotent stem cell (iPSC) derived cardiomyocytes treated with doxorubicin, both PLCE1 and

278 After birth cardiomyocytes undergo terminal differentiation, charact

279 When coupled to spontaneously beating cardiomyocytes via connexin-43-containing gap junctions,

280 regulator of cell viability and apoptosis in cardiomyocytes via simultaneous activation of p53 and ca

281 Force development in membrane-permeabilized cardiomyocytes was reduced because of decreased myofibri

282 Increased diastolic Ca(2+) release in wt-PMI cardiomyocytes was related to hyperphosphorylation of ry

283 The reduction of Ito currents in UNx EPI cardiomyocytes was secondary to downregulation of KChIP2

284 -T cells and cMy-mOVA mice expressing OVA on cardiomyocytes were crossed.

285 In addition, H9C2 rat cardiomyocytes were cultured in vitro and the phosphoryl

286 METHODS AND hiPSC cardiomyocytes were derived from a CPVT2 patient (D307H-

287 We found that TLR3- and STAT1-deficient cardiomyocytes were not more susceptible to Coxsackie vi

288 Cardiomyocytes were stretched to investigate titin diste

289 ced Ca(2+)-release events in the CPVT2-hiPSC cardiomyocytes when compared with healthy control cells.

290 th enhanced Kir2.1 expression and mouse HL-1 cardiomyocytes with ectopic expression of K2P1 channels

291 m 1 of Kir2 (Kir2.1) channels and mouse HL-1 cardiomyocytes with ectopic expression of two pore-domai

292 Suppressing the mitophagy pathway in HL-1 cardiomyocytes with either small interfering RNA (siRNA)

293 the hypothesis, we treated murine atrial HL1 cardiomyocytes with increasing doses of homocysteine or

294 tnatal myocardium, including: (1) rod-shaped cardiomyocytes with M bands assembled as a functional sy

295 Herein, we demonstrated that stimulation of cardiomyocytes with phenylephrine (PE), a well known hyp

296 iew cytosolic and nuclear Ca(2+) dynamics in cardiomyocytes with respect to their impact on Ca(2+)-de

297 itionally, pHi is elevated in Slc26a6(-/)(-) cardiomyocytes with slower recovery kinetics from intrac

298 terns are pivotal characteristics of failing cardiomyocytes, with several excitation-transcription co

299 sulted in a modest increase in c-kit-derived cardiomyocytes, with significant increases in the number

300 mental properties of ECC couplons in beating cardiomyocytes without pharmacological interventions.