ライフサイエンスコーパス: cardiomyocyte

1 complex regulate nuclear homeostasis in the cardiomyocyte.

2 pport electromechanical synchronicity within cardiomyocytes.

3 of AMPKbeta2 abrogates differentiation into cardiomyocytes.

4 sed mitochondrial proton permeability in old cardiomyocytes.

5 g downstream of beta-adrenergic receptors in cardiomyocytes.

6 f PCSK6 on mRNA and protein level in hypoxic cardiomyocytes.

7 d CHD genetics-in discrete subpopulations of cardiomyocytes.

8 tly confined to the T-tubules of healthy rat cardiomyocytes.

9 human induced pluripotent stem cell-derived cardiomyocytes.

10 terial, including mitochondria, derived from cardiomyocytes.

11 construct a mechanical microenvironment for cardiomyocytes.

12 ondrial distribution and function like adult cardiomyocytes.

13 the current approaches to mature PSC-derived cardiomyocytes.

14 ting on the top (dorsal) surface of cultured cardiomyocytes.

15 d perhaps distinct effects of hypokalemia on cardiomyocytes.

16 cRNA) exclusively expressed in primate fetal cardiomyocytes.

17 rine-induced hypertrophic growth in cultured cardiomyocytes.

18 ly demonstrated the regenerative capacity of cardiomyocytes.

19 gh spatiotemporal sensitivity on contracting cardiomyocytes.

20 m differentiation of embryonic stem cells to cardiomyocytes.

21 and Nrf2 was observed both in PBMCs and AC16 cardiomyocytes.

22 of the stimulus-dependent palmitoylation in cardiomyocytes.

23 arison with Diclofenac in immortalized human cardiomyocytes.

24 s to other cell types, including neurons and cardiomyocytes.

25 ction system (CCS), a specialized network of cardiomyocytes.

26 etabolism, thereby leading to ferroptosis in cardiomyocytes.

27 hown that cNCCs can also give rise to mature cardiomyocytes.

28 teins and localizes to intercalated discs in cardiomyocytes.

29 ntaneously contract faster than working-type cardiomyocytes.

30 s with newly designed gating properties into cardiomyocytes.

31 human induced pluripotent stem cell-derived cardiomyocytes.

32 and epitopes of cardiac proteins in isolated cardiomyocytes.

33 B(R120G)-expressing neonatal rat ventricular cardiomyocytes.

34 ced lateralization of Cx43 in isolated adult cardiomyocytes.

35 ws investigation of the secretome of primary cardiomyocytes.

36 n of FAO prevents the hypertrophic growth of cardiomyocytes.

37 2P)) channel family-are found in neurons(1), cardiomyocytes(2-4) and vascular smooth muscle cells(5),

38 cumulation of lipid vacuoles within knockout cardiomyocytes; (3) Hypoxia-inducible factor 1alpha prot

39 the challenge of attaining high densities of cardiomyocytes-a notoriously nonproliferative cell type.

40 tes, and that cyclic contractile activity of cardiomyocytes accelerates TT diffusion dynamics.

41 In rat cardiomyocytes, AKAP6 anchors centrosomal proteins to th

42 -clamp) and [Ca(2+)](i)-recordings in atrial cardiomyocytes, along with protein-expression levels in

43 maturation of pluripotent stem cell-derived cardiomyocyte and novel therapeutic strategies for heart

44 porating iron oxide nanoparticles into human cardiomyocytes and applying a short-term external magnet

45 se model of DCM in which they delete Lmna in cardiomyocytes and discover that bromodomain and extrate

46 DNA methylation in the normal homeostasis of cardiomyocytes and during cardiac stress, which could ma

47 n is essential for karyokinesis in mammalian cardiomyocytes and heart regeneration.

48 TAF overexpression down-regulated NEDD4-2 in cardiomyocytes and HEK cells.

49 bout the physiological role of polyploidy in cardiomyocytes and how this might relate to renewal and

50 and functional maturation of neonatal mouse cardiomyocytes and human embryonic stem cell-derived car

51 ion and structure was assessed in HL1 murine cardiomyocytes and human induced pluripotent stem cell-d

52 ings highlight the important role of LMNA in cardiomyocytes and identify BET bromodomain inhibition a

53 and Nav1.5 surface protein levels in rabbit cardiomyocytes and in HEK cells stably expressing Nav1.5

54 A-carboxylase 2) in phenylephrine-stimulated cardiomyocytes and in pressure overload-induced cardiac

55 CYP2J2 expression in human adult ventricular cardiomyocytes and interrogated whole genome transcripti

56 lterations in gene expression of ventricular cardiomyocytes and leads to the activation of a diverse

57 OPD-Pep delivered persulfides/H(2) S to H9C2 cardiomyocytes and lowered ROS levels as confirmed by qu

58 As to monitor electromechanical behaviors of cardiomyocytes and neurons.

59 udy is the first to show that fusion between cardiomyocytes and non-cardiomyocytes, identified by the

60 identifying major cell types, including both cardiomyocytes and noncardiomyocytes, on the basis of th

61 ted inhibited mitochondrial Ca(2+) uptake in cardiomyocytes and partial protection from ischemia-repe

62 s the potential to directly replicate within cardiomyocytes and pericytes, leading to viral myocardit

63 age in heterogeneous subsets of iPSC-derived cardiomyocytes and predicts candidate GRNs for human CHD

64 the structural and functional properties of cardiomyocytes and present the current approaches to mat

65 cRNA, BANCR, is primarily expressed in fetal cardiomyocytes and promotes cell migration.

66 entiation, as indicated by no or few beating cardiomyocytes and reduced expression of cardiomyocyte-s

67 the relationship between the redox state of cardiomyocytes and their mechanical microenvironment rem

68 Experiments were conducted in isolated human cardiomyocytes and trabeculae.

69 usion is affected by the mechanical state of cardiomyocytes, and that cyclic contractile activity of

70 Kynurenine precipitates cardiomyocyte apoptosis through reactive oxygen species

71 When compared to wild-type (WT) cardiomyocytes, ARDKO displayed reduced fractional short

72 Other cellular compartments in addition to cardiomyocytes are addressed, notably the coronary micro

73 ocytes and human embryonic stem cell-derived cardiomyocytes are considerably enhanced upon co-culture

74 In adult mammals, cardiomyocytes are traditionally considered to be termin

75 metabolic, and functional specializations in cardiomyocytes as the heart transits from fetal to adult

76 o in situ investigate the redox mechanism of cardiomyocytes at a single-cell level.

77 Conversely, deletion of Gfat1 in cardiomyocytes attenuates pathological cardiac remodelin

78 increasing crowding within the compact layer cardiomyocytes augments delamination, whereas decreasing

79 Cardiomyocyte beta(3)-adrenoceptors (beta(3)-ARs) couple

80 ent networks of macrophages, fibroblasts and cardiomyocytes between atria and ventricles that are dis

81 ell coculture did not significantly increase cardiomyocyte binucleation, suggesting that cFbs inhibit

82 d reversible conduction block that occurs in cardiomyocytes both result from bifurcations engendered

83 luble ubiquitinated proteins in CryAB(R120G) cardiomyocytes but did not alter autophagic flux.

84 oatings, which did not induce hypertrophy in cardiomyocytes, but allowed response to hypertrophic as

85 We established a novel secretome analysis of cardiomyocytes by combining stable isotope labeling and

86 driven transcription is re-engaged in mature cardiomyocytes by elevating levels of the positive trans

87 Knocking out Ube2v1 exclusively in cardiomyocytes by using AAV9 (adeno-associated virus 9)

88 stimulates cardiomyocyte proliferation in P2 cardiomyocytes, by activating insulin-like growth factor

89 sts that human pluripotent stem cell-derived cardiomyocytes can affect "heart regeneration", replacin

90 PSC-derived cardiomyocytes can be generated routinely with high yiel

91 mounting that proliferation of pre-existing cardiomyocytes can be stimulated to repair injury of the

92 sion of signaling pathways that regulate the cardiomyocyte cell cycle and advances in stem cell techn

93 mechanistically show that Pkm2 regulates the cardiomyocyte cell cycle and reduces oxidative stress da

94 portantly, boron has the potential to induce cardiomyocyte cell cycle entry and potentially cardiac t

95 ndogenous cardiac regeneration by triggering cardiomyocyte cell cycle reentry in the adult mammalian

96 st 2 decades, numerous studies have explored cardiomyocyte cell cycle regulatory mechanisms to enhanc

97 myocardial infarction, resulted in increased cardiomyocyte cell division, enhanced cardiac function,

98 chanisms in Long-Evans rat heart and in HL-1 cardiomyocyte cell line.

99 gnificant barrier to clinical translation of cardiomyocyte cell therapies for heart disease.

100 were derived from alterations in the grafted cardiomyocyte characteristics.

101 AC-Seq), we first find that the regenerating cardiomyocyte chromatin accessibility landscape undergoe

102 e profiling of 21,422 single cells-including cardiomyocytes (CMs) and non-CMs (NCMs)-from normal, fai

103 e is known about the intrinsic effect on the cardiomyocytes (CMs).

104 epridil's more proarrhythmic action in adult cardiomyocytes compared to hiPSC-CMs could be traced to

105 )1.2 is regulated by different mechanisms in cardiomyocytes compared to neurons and vascular smooth m

106 n, increased fibrosis, and lateralization of cardiomyocyte connexin-40.

107 n improvement of cardiac function as well as cardiomyocyte contractility and reduction in adverse ven

108 rganism swimming performance/respiration and cardiomyocyte contractility dynamics in mahi-mahi (Coryp

109 Thus, human cardiomyocyte contractility model could accurately facil

110 we sought to develop an adult human primary cardiomyocyte contractility model that has the potential

111 kinase acting upon RLC, in the regulation of cardiomyocyte contractility remains poorly understood.

112 Additionally, [Na(+)](o) modulates cardiomyocyte contractility via a sodium-calcium exchang

113 sins in the DRX conformation, which enhanced cardiomyocyte contractility, but impaired relaxation and

114 We next probed effects on human cardiomyocyte contractility.

115 Cardiomyocyte culture studies using multielectrode array

116 ly recorded spontaneous action potentials in cardiomyocytes, cultured hippocampal and dorsal root gan

117 rdiac ECM as a nonpermissive environment for cardiomyocyte cytokinesis and uncovered novel functions

118 e binucleation, suggesting that cFbs inhibit cardiomyocyte cytokinesis through ECM modulation rather

119 d NPNT (nephronectin) in promoting postnatal cardiomyocyte cytokinesis.

120 Cardiomyocyte death and heart damage was due to pneumoly

121 Thus, cardiomyocyte death as occurs during myocardial infarcti

122 so directly causes mitochondrial rupture and cardiomyocyte death during ischemia-reperfusion injury b

123 hila L(2)gl, Llgl1 depletion in cultured rat cardiomyocytes decreased Yap protein levels and blunted

124 ion of gene expression programs that promote cardiomyocyte dedifferentiation, proliferation, and prot

125 Cardiomyocytes derived from human induced pluripotent st

126 We also used cardiomyocytes derived from human pluripotent stem cells

127 titial fibrosis, cardiomyocyte myocytolysis, cardiomyocyte diameter, glycogen score or Cx43 distribut

128 CITED4 deletion in cardiomyocytes did not affect baseline cardiac size or f

129 ion factor, TBX5, in individual cells during cardiomyocyte differentiation from human induced pluripo

130 function (LoF) and missense variants during cardiomyocyte differentiation of isogenic human induced

131 specific regulatory region activated during cardiomyocyte differentiation that binds to the ACTN2 ge

132 fferentiated cell pluripotency but inhibited cardiomyocyte differentiation, as indicated by no or few

133 ole of lncRNA GATA6-AS1 in controlling human cardiomyocyte differentiation.

134 tively few have been shown to regulate human cardiomyocyte differentiation.

135 These proliferative neonatal cardiomyocytes display a unique transcriptional program

136 MdxS3E cardiomyocytes displayed improved intracellular Ca2+ sig

137 ls play a critical role in repolarization of cardiomyocytes during the cardiac action potential (AP).

138 s of all major cardiac cell types, including cardiomyocytes, endothelial cells, fibroblasts, and macr

139 Failing cardiomyocytes exhibit elevated viscosity and reducing m

140 pport the hypothesis that immortalized human cardiomyocytes exposed to Ketoprofen are subjected to to

141 Additionally, cardiomyocyte exposures to the same HF-FW sample at 2% d

142 Cardiomyocytes, fibroblasts, and endothelial cells attac

143 Fisetin enhances viability of rat cardiomyocytes following hypoxia/starvation - reoxygenat

144 on and leveraging them to create more mature cardiomyocytes for research and regenerative medicine.

145 d be utilised to drive regeneration of adult cardiomyocytes for the treatment of heart myopathies.

146 on-contraction coupling (ECC) in ventricular cardiomyocytes from a previously characterized mouse mod

147 y) and SERCA2a downregulation in ventricular cardiomyocytes from C-dnO1 mice, associated with blunted

148 Current differentiation protocols to produce cardiomyocytes from human induced pluripotent stem cells

149 In primary cardiomyocytes from human infants with heart disease, mo

150 Currents were recorded in cardiomyocytes from mice trans-expressing human WT or p.

151 ecific induced pluripotent stem cell-derived cardiomyocytes from NS patients carrying biallelic varia

152 n HF, with dramatically slowed relaxation in cardiomyocytes from patients with HF with preserved ejec

153 t to lower stiffness and speed relaxation in cardiomyocytes from patients with HF, supporting further

154 altered transcriptional networks may impact cardiomyocyte function and ionic currents that impact AF

155 and genes associated with heart development, cardiomyocyte function, and CHD genetics-in discrete sub

156 ure with left ventricular dilation, impaired cardiomyocyte growth accompanied by reduced mTOR (mammal

157 ), the rate-limiting enzyme of HBP, promotes cardiomyocyte growth.

158 Knockout of DNMT3A in human cardiomyocytes had three main consequences for cardiomyo

159 trophic cardiomyopathy where misalignment of cardiomyocytes has been observed in utero.

160 howed that human embryonic stem cell-derived cardiomyocytes (hESC-CMs) contain nodal-like cardiomyocy

161 brosis, with ischaemia indicated by enhanced cardiomyocyte Hif1a expression.

162 human induced pluripotent stem cell-derived cardiomyocyte (hiPSC-CM) technology and by contact-free

163 human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) in vitro can expand CMs modes

164 human induced pluripotent stem cell derived cardiomyocytes (hiPSC-CMs) is a major limitation to the

165 Human-induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) provide an excellent platform

166 human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs), and we describe responses to

167 has been shown to potentate I(to) in canine cardiomyocytes; however, its effects on I(to) in other s

168 e drugs, human pluripotent stem cell-derived cardiomyocytes (hPSC-CMs) have been proposed as a therap

169 cardiac function and energetics, and reduces cardiomyocyte hypertrophy during cardiac stresses.

170 Although cardiomyocyte hypertrophy is often associated with these

171 ass IIa histone deacetylases (HDACs) repress cardiomyocyte hypertrophy through association with the p

172 n the LV weight-to-tibia length ratio due to cardiomyocyte hypertrophy.

173 a causal role of elevated aspartate level in cardiomyocyte hypertrophy.

174 w that fusion between cardiomyocytes and non-cardiomyocytes, identified by the SP phenotype, contribu

175 oss-of-function studies of HDAC7 in cultured cardiomyocytes implicated HDAC7 as a prohypertrophic sig

176 human induced pluripotent stem cell-derived cardiomyocytes in cardiac microtissue and single-cell as

177 sed in mouse hearts after MI and in isolated cardiomyocytes in response to hypertrophic and inflammat

178 es, and subsequently differentiate them into cardiomyocytes in situ.

179 omyopathy (DMCM) may involve lipotoxicity of cardiomyocytes in the context of hyperglycemia.

180 cell-derived cardiomyocytes that mimic fetal cardiomyocytes in vitro to discover hundreds of ERV tran

181 icals, multispecific drugs, the targeting of cardiomyocyte inflammatory signaling and potential consi

182 owever, the molecular signature of the adult cardiomyocytes involved in this repair is unclear.

183 d that induced pluripotent stem cell-derived cardiomyocytes (iPSC-CMs) from patients with a dilated c

184 However, its role in the cardiomyocyte is undefined.

185 SK2 channels in hypertrophic rat ventricular cardiomyocytes is driven by protein kinase A (PKA) phosp

186 sue symmetry is broken to specify trabecular cardiomyocytes is unknown.

187 ion defects in pluripotent stem cell-derived cardiomyocyte, its antagonistic effect on myocardial reg

188 min B2, a nuclear lamina filament supporting cardiomyocyte karyokinesis, also facilitates cell divisi

189 ncing via RNA-DNA triple helix formation and cardiomyocytes lacking the triple helix forming domain o

190 In membrane-permeabilized Casq2-/- cardiomyocytes-lacking intact sarcolemma and devoid of s

191 tion of 14-3-3 to beta-adrenergic-stimulated cardiomyocytes led to prolonged SERCA activation, presum

192 gated whether beta-adrenergic stimulation of cardiomyocytes led to stimulus-dependent palmitoylation

193 Paradoxically, cell therapies to offset cardiomyocyte loss after ischemic injury improve long-te

194 t cardiovascular event and a major cause for cardiomyocyte loss.

195 is1 and Hoxb13 act cooperatively to regulate cardiomyocyte maturation and cell cycle.

196 escent reporter system for the assessment of cardiomyocyte maturation and identified potent maturatio

197 we review the major hallmarks of ventricular cardiomyocyte maturation and summarize key regulatory me

198 Cardiomyocyte maturation gained increased attention rece

199 ical targeting of which substantially delays cardiomyocyte maturation in postnatal hearts, and marked

200 advances in the technical platforms used for cardiomyocyte maturation research, we expect significant

201 n required for cardiac nerve development and cardiomyocyte maturation soon after birth.

202 single-cell analysis of in vivo and in vitro cardiomyocyte maturation trajectories identify highly co

203 onstituent in the microenvironment promoting cardiomyocyte maturation, providing insights into how th

204 re generally used to determine the status of cardiomyocyte maturation, they could be time-consuming a

205 om a neonatal to adult state and this drives cardiomyocyte maturation.

206 diomyocytes to a quiescent state and enhance cardiomyocyte maturation.

207 the contributions of the microenvironment to cardiomyocyte maturation.

208 viding insights into how the manipulation of cardiomyocyte maturity may impact on disease development

209 Immaturity of iPSC-derived cardiomyocytes may be a significant barrier to clinical

210 thors compared DMD and control hiPSC-derived cardiomyocytes, mdx mice, and control mice (in the prese

211 outward K(+) currents that are critical for cardiomyocyte membrane repolarization.

212 se assay) and was downregulated in AF atrial cardiomyocytes; microRNA-26a silencing reproduced AF-ind

213 13 double-knockout hearts display widespread cardiomyocyte mitosis, sarcomere disassembly and improve

214 Computer simulations using a rabbit-cardiomyocyte model demonstrated that changes in Ca(2+)

215 In an LQT type 1 (LQT1) cardiomyocyte model, enDUB treatment restored delayed re

216 assays can be complex, and the use of hiPSC-cardiomyocyte models of congenital disease phenotypes fo

217 We evaluated cardiomyocyte morpho-pathology by seriated biopsies of h

218 rdiomyocytes had three main consequences for cardiomyocyte morphology and function: (1) Gene expressi

219 The extent of atrial interstitial fibrosis, cardiomyocyte myocytolysis, cardiomyocyte diameter, glyc

220 damage incurred during IPD is due in part to cardiomyocyte necroptosis.

221 myocardium, dendritic cells (DC) respond to cardiomyocyte necrosis, present cardiac antigen to T cel

222 nd contractility of neonatal rat ventricular cardiomyocytes (NRVCMs) cultured on these sheets.

223 crease in cardiomyocyte volume but decreased cardiomyocyte nuclear density in the left ventricle.

224 AF increases atrial-cardiomyocyte nucleoplasmic [Ca(2+)] by IP(3)R1-upregula

225 RV fibroblasts but not in LV fibroblasts nor cardiomyocytes of either ventricle.

226 e scale triggers tension heterogeneity among cardiomyocytes of the compact layer and drives those wit

227 ecific endothelial or smooth muscle cells or cardiomyocyte or myeloid cell deficiency of IDO and chal

228 Mice lacking cardiomyocyte PAM (Pam (Myh6-cKO/cKO)) are viable, but a

229 on, this effect can be attributed to an EpAT-cardiomyocyte paracrine axis.

230 modification of titin, UnDOx modulates human cardiomyocyte passive force bidirectionally.

231 zebrafish resulted in larger and dysmorphic cardiomyocytes, pericardial effusion, impaired blood flo

232 cardiomyocytes, raising the hypothesis that cardiomyocyte polyploidy poses a barrier for cardiomyocy

233 iPSCs) are capable of generating highly pure cardiomyocyte populations as determined by expression of

234 We also report that human hiPSC-derived cardiomyocytes possess measurable TRPM7 currents; howeve

235 In voltage-clamped, intact Casq2-/- cardiomyocytes pretreated with tetrodotoxin to inhibit s

236 n in postnatal hearts, and markedly enhances cardiomyocyte proliferation and improves cardiac functio

237 Endocardial abnormalities cause reduced cardiomyocyte proliferation and maturation by disrupting

238 cardiomyocyte polyploidy poses a barrier for cardiomyocyte proliferation and subsequent heart regener

239 crosstalk with other pathways implicated in cardiomyocyte proliferation calls for the identification

240 of nodal points in the cell signaling before cardiomyocyte proliferation can be moved forward toward

241 wly-identified component of ICDs, results in cardiomyocyte proliferation defects and cardiomyopathy.

242 at exogenous thyroid hormone (T3) stimulates cardiomyocyte proliferation in P2 cardiomyocytes, by act

243 e different signaling pathways implicated in cardiomyocyte proliferation with emphasis on wingless/in

244 potassium channel at the plasma membrane of cardiomyocytes prolongs action potential repolarization,

245 in the use of pluripotent stem cell-derived cardiomyocytes (PSC-CMs) for both patient health and sci

246 Pluripotent stem cell-derived cardiomyocytes (PSC-CMs) hold great promise for disease

247 erative capacity dominantly comprise diploid cardiomyocytes, raising the hypothesis that cardiomyocyt

248 ons affect the timing or function of CFRI in cardiomyocytes remain open questions that are discussed

249 ver, the cell-specific role of BRD4 in adult cardiomyocytes remains unknown.

250 schemic episodes lead to a global pattern of cardiomyocyte remodeling and dedifferentiation, hallmark

251 Cx43 redistribution to the lateral sides of cardiomyocytes (remodeling).

252 t (I (Ks) ), which is partly responsible for cardiomyocyte repolarization and physiologic shortening

253 iption factors play an essential role in the cardiomyocyte response to injury by regulating chromatin

254 f diabetic cardiomyopathy was confirmed by a cardiomyocyte-restricted (CR) Nrf2 transgenic approach i

255 -CMs (induced pluripotent stem cells derived cardiomyocytes) show hypercontractility, increased metab

256 The fibrosis-entrapped cardiomyocytes showed sarcolemmal damage and connexin 43

257 Heart size and weight, cardiomyocyte size, and cardiac fibrosis were increased

258 Cardiomyocyte-specific CatA overexpression and increased

259 We generated cardiomyocyte-specific CITED4 knockout mice (C4KO) and s

260 ology, a transgenic mouse was generated with cardiomyocyte-specific expression of an ion pore-disrupt

261 Similarly, constitutive cardiomyocyte-specific KLF5 overexpression caused cardia

262 Cardiomyocyte-specific MCUb overexpressing transgenic mi

263 In addition, using cardiomyocyte-specific Pkm2 modified RNA, our novel card

264 ing cardiomyocytes and reduced expression of cardiomyocyte-specific proteins.

265 Inducible cardiomyocyte-specific Tjp1 deletion mice (Tjp1(fl/fl);

266 Passive cardiomyocyte stiffness was reduced by chronic PDE9a inh

267 In the perinatal period, cardiomyocytes still proliferate, and the heart shows th

268 proliferative capacity of the differentiated cardiomyocyte: studies in zebrafish and neonatal mammals

269 %ID/g, P = 0.006), though the efficiency of cardiomyocyte suppression was variable among TAC mice.

270 is downregulated by aging, as a regulator of cardiomyocyte survival.

271 Isolated atrial cardiomyocytes tachypaced at 3 Hz for 24 hours mimicked

272 yocyte-specific Pkm2 modified RNA, our novel cardiomyocyte-targeted strategy, after acute or chronic

273 We identify immature cardiomyocytes that enter the cell cycle following injur

274 we use primate pluripotent stem-cell-derived cardiomyocytes that mimic fetal cardiomyocytes in vitro

275 cardiomyocytes (hESC-CMs) contain nodal-like cardiomyocytes that spontaneously contract faster than w

276 and mechanically interrogating iPSC-derived cardiomyocytes, the initial results indicate that this a

277 d pathological program toward ferroptosis in cardiomyocytes, thereby worsening the progression of dia

278 calcium current decreases versus 1-Hz-paced cardiomyocytes; these changes were prevented by IP(3)R k

279 ion of the mTOR-signaling pathway could lead cardiomyocytes to a quiescent state and enhance cardiomy

280 hors used DMD patient-specific hiPSC-derived cardiomyocytes to examine the physiological response to

281 These molecular substrates sensitize cardiomyocytes to spontaneous Ca(2+)-releases and arrhyt

282 ing the AP in rabbit and porcine ventricular cardiomyocytes to test our hypothesis that the balance b

283 The application of dCas9 to activate cardiomyocyte transcription in targeted genomic loci in

284 In cultured cardiomyocytes, treatment with the FOXO1 inhibitor AS184

285 aping action potentials (APs) in ventricular cardiomyocytes under beta-adrenergic stimulation or in d

286 a(2+) ) transients were measured in isolated cardiomyocytes under field stimulation or patch clamp.

287 During development, cardiomyocytes undergo a shift from a proliferative stat

288 ut is lost during postnatal development when cardiomyocytes undergo cell-cycle arrest and polyploidiz

289 In vivo, cardiomyocytes undergo numerous adaptive structural, fun

290 d diastolic dysfunction, with an increase in cardiomyocyte volume but decreased cardiomyocyte nuclear

291 crotubules as a source of viscoelasticity in cardiomyocytes, we sought to test whether microtubules c

292 Neonatal rat ventricular cardiomyocytes were infected with adenoviruses expressin

293 Atrial cardiomyocytes were isolated from control and AF dogs (k

294 n-expression levels in tissue homogenates or cardiomyocytes, were assessed in 265 atrial samples from

295 calization of endogenous LITAF and Nav1.5 in cardiomyocytes, whereas co-immunoprecipitations confirme

296 Furthermore, incubation of cardiomyocytes with 12,13-diHOME increased mitochondrial

297 far from being able to generate PSC-derived cardiomyocytes with adult-like phenotypes in vitro.

298 xes function as tubulin carboxypeptidases in cardiomyocytes, with a predominant role for VASH1.

299 Cardiomyocyte Yap protein levels were decreased in llgl1

300 difications of MTs have differing effects on cardiomyocyte YM: Acetylation provides flexibility, wher