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1 nel 6, which has been implicated in podocyte calcium handling.
2 including diastolic dysfunction and impaired calcium handling.
3 eling of excitation-contraction coupling and calcium handling.
4 ed cytochrome oxidase activity and defective calcium handling.
5 sphorylation (S16), consistent with improved calcium handling.
6 l relaxation resulting from abnormal myocyte calcium handling.
7 -induced VT/VF under conditions of defective calcium handling.
8 associated with alterations in intracellular calcium handling.
9 function, leading to disturbed intracellular calcium handling.
10 on, myocardial energetics, and intracellular calcium handling.
11 activity is decreased, resulting in abnormal calcium handling.
12 likely indicating improvement in myocellular calcium handling.
13 ed these effects to changes in intracellular calcium handling.
14 consistent with markedly abnormal myocardial calcium handling.
15 allmark changes in cardiac contractility and calcium handling.
16 OS), mitochondrial dysfunction, and abnormal calcium handling.
17 uctural integrity, contractile function, and calcium handling.
18 n the cells' action-potential morphology and calcium handling.
19 c and imply that this is related to improved calcium handling.
20 an provide a surrogate measure of myocardial calcium handling.
21 owed reduced dendrite length and deficits in calcium handling.
22 tudies in hypertension and the regulation of calcium handling.
23 ty due to modulated cardiolipin and improved calcium handling.
24 ted to extracellular matrix organization and calcium handling.
25 t SPEG is critical for triad maintenance and calcium handling.
26 n network synchrony, dendrite outgrowth, and calcium handling.
27 o need to postulate defects in intracellular calcium handling.
28 r cardiomyocytes exhibited markedly improved calcium handling.
29 ted with alterations in proteins involved in calcium handling.
30 ll EP by changing both membrane currents and calcium handling.
31 keletal proteins, and proteins that regulate calcium handling.
32 ium release channel regulation, and cellular calcium handling.
33 s for alterations in cellular morphology and calcium handling.
34 disrupted transverse tubule organization and calcium handling.
35 g human hearts are characterized by abnormal calcium handling, a negative force-frequency relationshi
36 y regulating the intracellular structure and calcium handling ability.
37 sarcomeric length, gap junction protein, and calcium-handling ability in coculture with ECs.
38 vious work showing that saturated fat causes calcium handling abnormalities in cardiomyocytes, we hyp
39 the molecular phenotype and normalization of calcium-handling abnormalities.
40 e deficit in AAA cardiomyocytes, but not the calcium-handling abnormalities.
41 including cell survival, cytokine signaling, calcium handling, adrenergic receptor signaling, cytoske
42                            Altered muscle SR calcium handling also rendered these mice exercise intol
43 ersensitivity, which may include receptor or calcium-handling alterations within the vasculature.
44  cardiac dysfunction, dampened intracellular calcium handling, alterations in cardiac morphology, and
45 s in part mediated by abnormal mitochondrial calcium handling and a decreased level of free matrix ca
46 ation, repolarisation, arrhythmia detection, calcium handling and beat-to-beat heterogeneity.
47 was accompanied by improved hemodynamics and calcium handling and by reduced inflammation, hypertroph
48 ting possibility that sarcoplasmic reticulum calcium handling and cardiac contractility may be regula
49 ed pathways linked to abnormal intracellular calcium handling and cardiac neurotransmission.
50 ort and cell cycle genes, leading to altered calcium handling and cell cycle defects.
51                      NO is known to modulate calcium handling and cellular signaling in the myocardiu
52 activity is decreased, resulting in abnormal calcium handling and contractile dysfunction.
53 d to functional alterations in intracellular calcium handling and contractile function.
54                       Functional analysis of calcium handling and contractile parameters in isolated
55  by increased myofiber diameter and improved calcium handling and contractile strength.
56 vity was measured as an index of myocellular calcium handling and coupled to its regulation via the p
57 ar O-GlcNAcylation has beneficial effects on calcium handling and diabetic cardiac function.
58 protein turnover, intracellular trafficking, calcium handling and electrical excitability - processes
59 hat loss of PKP2 expression affects cellular calcium handling and electrophysiology differently in le
60 ical genes involved in contractile function, calcium handling and energy metabolism underpins this co
61                                Properties of calcium handling and exchanger currents are altered to a
62 ral and transchamber expression gradients of calcium handling and gap junction proteins that may wors
63 se 2a (SERCA2a) in the regulation of overall calcium handling and heart muscle contractility.
64 r of contractile function through effects on calcium handling and hypertrophy through protein kinase
65                   There were also changes in calcium handling and in action potential waveforms, and
66 gnaling events would be predicted to promote calcium handling and increase contractile function of th
67 ad to proteasome impairment, such as altered calcium handling and increased oxidative stress due to m
68 cal approaches can therapeutically rebalance calcium handling and inhibit arrhythmia.
69 m ATPase (SERCA) plays a key role in cardiac calcium handling and is considered a high-value target f
70                 To study the effect of VF on calcium handling and its modulation by dantrolene, heart
71                                     Although calcium handling and myofibrillar proteins have been imp
72  effects are modulated by phosphorylation of calcium handling and myofilament proteins such as tropon
73 s may produce heterogeneity of intracellular calcium handling and pacemaker activity across the SAN.
74 evaluated protein expression associated with calcium handling and pacemaker-nodal expression.
75 RF in this cardiomyopathy and its effects on calcium handling and PLN aggregation.
76 ontributing to HCM, including alterations of calcium handling and proteolysis, microtubule modificati
77 tensively characterized, through analysis of calcium handling and response to beta-agonist.
78 of SR Ca(2+)-ATPase can modify intracellular calcium handling and shortening in myocardial cells.
79  changes to synaptic and neuronal structure, calcium handling and the balance of excitatory and inhib
80 protection against maladaptive cardiomyocyte calcium handling and thereby improvement in cardiac func
81 -dependent cardiovascular functions, such as calcium handling and vascular tone.
82      However, heterogeneity of intracellular calcium handling and, in particular, its effect on the e
83 es in gene expression, myocyte architecture, calcium handling, and contractile function and compared
84 s accompanied by myofibril disarray, altered calcium handling, and differential alternative splicing
85 pecific information on ion channel kinetics, calcium handling, and dynamic changes in the intracellul
86                                 Contraction, calcium handling, and electrophysiology experiments were
87 ad drive maturation of contractile function, calcium handling, and electrophysiology.
88  to changes in sarcomeric proteins, abnormal calcium handling, and fibrosis.
89                           Action potentials, calcium handling, and ion currents were recorded in vent
90          Furthermore, respiratory variables, calcium handling, and membrane potentials of synaptosome
91 ense mutation showed impaired contractility, calcium handling, and metabolic activity.
92 roved the cells' mitochondrial structure and calcium handling, and observed divergent cell-source-dep
93 lectrophysiology, dysregulated intracellular calcium handling, and proarrhythmic behavior in isolated
94 ce-frequency and force-length relationships, calcium handling, and responses to beta-adrenergic agoni
95 tive phosphorylation, fatty acid metabolism, calcium handling, and sarcomere function, and the activa
96  and altered expression of genes involved in calcium handling, angiogenesis, and glucose metabolism.
97 gressively impaired contractile function and calcium handling, apoptosis, and sarcomere disarray.
98     Remarkable new roles for mitochondria in calcium handling, apoptosis, heme turnover, inflammation
99     We conclude that cardiac ion channel and calcium handling are abnormal in CKD rats, leading to in
100             Mitochondrial ATP production and calcium handling are critical for metabolic regulation a
101                           The alterations in calcium handling are due at least in part to direct down
102 S production and impairment of mitochondrial calcium handling are key mechanisms of IR injury.
103 chanism whereby alterations in intracellular calcium handling are linked to the expression of hypertr
104 nt view is that instabilities in subcellular calcium handling are the main underlying mechanism.
105 fic inactivation of Tet2, we propose altered calcium handling as an arrhythmogenic mechanism, depende
106    Our results support network synchrony and calcium handling as outcomes directly linked to this gen
107 cardiomyocyte contractility and dysregulated calcium handling associated with high-fat diet.
108 lay fatigue development and improve myofibre calcium handling at a near-physiological oxygen tension.
109  pathological metabolic shifts, fibrosis and calcium handling) at the transcriptomic, structural and
110  decreased myocyte and myofilament function, calcium handling, beta-adrenergic responsiveness, mitoch
111 o potentiate the inhibition of cardiomyocyte calcium handling by amiodarone, which functions as a mul
112 ransition pore, we used an in vitro assay of calcium handling by isolated brain mitochondria.
113 th triadin suggest that HRCBP is involved in calcium handling by the SR.
114 use model appears to be related to decreased calcium handling by the SR.
115 stent with earlier results that indicate the calcium handling capacity of a range of tissues includin
116 n species (ROS) negatively affect myocardial calcium handling, cause arrhythmia, and contribute to ca
117  as fibrosis, cardiomyocyte hypertrophy, and calcium handling (Col1a2, Nppa, and Serca2).
118 reater contraction force, and alterations in calcium handling compared with wild-type iPSC-CMs.
119 dent adjustment of membrane excitability and calcium handling, compromising the enhancement of cardia
120 oliferation and for protein synthesis of the calcium handling constituents required for tissue contra
121 , we hypothesized that altered mitochondrial calcium handling contributes to dendritic retraction eli
122 tochondrial and metabolic function, impaired calcium handling, decreased antioxidant pathway activity
123                                              Calcium handling defects and perinuclear PLN aggregation
124                              Contractile and calcium handling defects were partly corrected by treatm
125 ncomitant with endoplasmic reticulum stress, calcium handling defects, and changes in the geometry an
126  (HF) is associated with impaired myocardial calcium handling, deficient SERCA2a, and increased susce
127 CMs with a homozygous PKP2 mutation also had calcium-handling deficits.
128  Podocyte depletion may result from improper calcium handling due to abnormal activation of the calci
129  physiological conditions, the complexity of calcium handling during systole and diastole has made th
130 rther, Brachyury priming drove maturation of calcium handling enabling transfected cells to maintain
131 er myofibril density and alignment, improved calcium handling, enhanced contractility, and more physi
132  has been shown to counteract PLN regulatory calcium handling function in the sarco/endoplasmic retic
133 rent ER compartments specialize in different calcium-handling functions (Ca(2+) release and Ca(2+) re
134 on and alternative splicing transitions, and calcium-handling functions are significantly enriched am
135 by marked reduction of energy/metabolism and calcium-handling gene expression (eg, PGC1-alpha, peroxi
136  (lncRNA) required for the expression of the calcium-handling gene Ryr2.
137 ioxidant system, B-adrenergic signaling, and calcium handling genes in the fetus and adult, in frozen
138  Pitx2 target genes that include channel and calcium handling genes, as well as genes that stabilize
139 ia on hECT-developed force and expression of calcium-handling genes (eg, SERCA2a, L-type calcium chan
140 magnesium-handling genes along DCT1 and more calcium-handling genes along DCT2.
141 lar drive train pattern on the expression of calcium-handling genes and proteins in rat ventricular m
142 sequencing to search for splicing changes in calcium-handling genes of HIF-PPN hearts and compared th
143 de of mitochondrial depolarization, aberrant calcium handling, impaired ATP synthesis, and activation
144 evated serum aldosterone levels, and altered calcium handling in a controlled experimental model of h
145 on of genes involved in lipid metabolism and calcium handling in cells of the peripheral nerve system
146 eling of excitation-contraction coupling and calcium handling in failing and nonfailing human hearts.
147  identify miRNAs that suppress intracellular calcium handling in heart muscle by interacting with mes
148  A signaling and was reversed for effects on calcium handling in HL-1 cells.
149 neity of excitation-contraction coupling and calcium handling in human hearts.
150 ed CFB transcriptional programs and improved calcium handling in human pluripotent stem cell-derived
151 analyses addressed cardiac contractility and calcium handling in isolated tissues and myocytes and an
152 estigate the arrhythmogenic role of abnormal calcium handling in many pathological settings.
153 tional modifications of proteins involved in calcium handling in myocytes, such as the cardiac ryanod
154                                              Calcium handling in pancreatic beta-cells is important f
155 c phenotype of these mice and that different calcium handling in PCs and type II UBCs may account for
156 hus thyroid hormone improves LV function and calcium handling in pressure overload hypertrophy, and t
157 ificantly reduced contractility and impaired calcium handling in response to ISO, which was reversed
158 an updated description of the key aspects of calcium handling in the kidney, focusing on the function
159                                      Altered calcium handling in these diseases is evidenced by chang
160 nsistent with a regulatory role for HRCBP in calcium handling in vivo and suggests that mutations in
161 ive splicing, myofibrillar organization, and calcium handling in zebrafish and human cardiomyocytes.
162 junctional membrane complex that facilitates calcium-handling in the cardiomyocyte.
163                     Changes in intracellular calcium handling, including a reduced activity of the sa
164 d that Pkd2(+/-) cardiomyocytes have altered calcium handling, independent of desensitized calcium-co
165 incipal role of mitochondria in pre-synaptic calcium handling is to take up Ca2+ directly or to fuel
166           This is due to profoundly abnormal calcium handling, leading to an inability to normalize c
167  6 had abnormal contraction, relaxation, and calcium handling (LVHdecomp).
168 ardial edema, suggesting abnormal myocardial calcium handling may be implicated in the pathophysiolog
169 contractile deficits alone without improving calcium handling may be insufficient for effective manag
170                                Intracellular calcium handling, measured by Rhod 2 spectrofluorometry,
171                                  Analyses of calcium-handling measures demonstrate that RanBP9 select
172 cardiac maturation, including contractility, calcium handling, metabolism, and hypertrophy.
173 heart muscle cells by boosting intracellular calcium handling might be an effective therapy.
174 pression of genes associated with signaling, calcium handling, mitochondria function and biogenesis,
175 hanges to the content of proteins related to calcium handling, mitochondrial quality control, reactiv
176          Forced expression of NCX1h or other calcium-handling molecules restored synchronized heartbe
177 onal relationship among proteins involved in calcium handling, myofibrils, and energy production may
178 d the contractility, myofibril structure and calcium handling of human engineered heart tissues, whil
179 ions in sarcomere genes may distinctly alter calcium handling pathways.
180 logical and pathophysiological intracellular calcium handling phenomena at the whole-cell.
181  as well, demonstrating the novel and unique calcium handling profile of TOT cardiomyocytes.
182  in the heart, which contributes to abnormal calcium handling, promoting arrhythmia.
183                   The mean contractility and calcium handling properties of cardiomyocytes isolated f
184 ium affects the anatomy, gene expression and calcium handling properties of trigeminal sensory affere
185                         We observed aberrant calcium handling properties with prolonged decay kinetic
186 intenance resulting in unique impairments in calcium handling properties.
187 r calcium signalling was recorded to compare calcium-handling properties among cardiomyocytes differe
188 action and relaxation with minimal effect on calcium-handling properties in vitro, and that contracti
189                              In conjunction, calcium-handling protein expression was examined in left
190 ocyte functions such as electrical activity, calcium handling, protein translation, and growth.
191                           Gene expression of calcium handling proteins (SERCA, phospholamban) and str
192  of gene expression and protein synthesis of calcium handling proteins compared to the 2D constructs
193 he gene expressions and protein synthesis of calcium handling proteins decreased significantly during
194                              Levels of these calcium handling proteins in SR get altered under diseas
195                             Although several calcium handling proteins that control differentiation o
196 rtrophic stimulus norepinephrine, only a few calcium handling proteins were differentially labeled fo
197 unction, expression of hypertrophic markers, calcium handling proteins, and cardiac fibrosis were the
198 AR pathway balance and changed expression of calcium handling proteins, which resulted in altered car
199 f beta1-adrenergic receptor (ADRB1) or other calcium handling proteins.
200 sponse to calcium that is independent of the calcium handling proteins.
201 logical roles of sarcoplasmic reticulum (SR) calcium handling proteins.
202 e in cardiomyocytes death and alterations in calcium handling proteins.
203 h sex-specific differences in the content of calcium handling proteins.
204 nregulation of mRNAs encoding sarcomeric and calcium handling proteins.
205 sed in Sgcg muscle focused on those encoding calcium-handling proteins and responsive to TGFbeta sinc
206                       Several other abnormal calcium-handling proteins in the failing heart are candi
207 reased cell capacity, and alterations in the calcium-handling proteins that were similar for RV free
208 anger function and phosphorylation levels of calcium-handling proteins were significantly decreased i
209 estigations, and examinations of connexin43, calcium-handling proteins, and histomorphology were carr
210       We investigated whether alterations in calcium-handling proteins, beta-adrenoceptor density, or
211 s sodium channels, transcription factors and calcium-handling proteins, but also point to previously
212 egulate PKA-dependent phosphorylation of key calcium-handling proteins, including the ICa,L-carrying
213  altering the expression and activity of key calcium-handling proteins.
214 changes were seen in the expression of other calcium-handling proteins.
215 tered myocyte calcium cycling and changes in calcium-handling proteins.
216 skeletal, nucleoskeletal, mitochondrial, and calcium-handling proteins.
217 ges in cardiac gene expression, and abnormal calcium handling-providing further evidence to establish
218 ffects of chronic CaSR activation on tubular calcium handling remain to be fully elucidated.
219 dverse structural, electrophysiological, and calcium handling remodeling that leads to patient morbid
220  in R92L animals led to worsened myocellular calcium handling, remodeling, and function.
221 rial morphology, transcriptional signatures, calcium handling, responses to hypoxia, neurohormonal st
222 ere correlated with changes in intracellular calcium handling, resulting in increased nitric oxide bi
223 says, e.g., to probe respiratory capacity or calcium handling, revealing cell-type-specific mitochond
224 to known gene expression changes, additional calcium-handling, sarcomeric, adrenergic signaling, and
225 cardiac remodeling as a result of changes in calcium handling, separate from renal complications.
226 sional tissue simulations with physiological calcium handling showed that tachycardia increased re-en
227 evels of some of the other genes involved in calcium handling, such as the ryanodine receptor and cal
228 s associated with progressive changes in the calcium handling system of atrial myocytes.
229 tion of impaired cardiac cAMP generation and calcium handling that result from AC6 deletion underlies
230 e, Ang-(1-9) directly affected cardiomyocyte calcium handling through a protein kinase A-dependent me
231 reduced in PPCM, affecting contractility and calcium handling through altered expression of PLN (phos
232  explain why SERCA gene therapy, a change in calcium handling to treat heart failure, might fail to i
233 te known sex differences in ion channels and calcium handling under normal sinus rhythm and AF condit
234 a-adrenergic-stimulated myocyte function and calcium handling, upregulating beta(1) receptors and ade
235           We aimed to investigate myocardial calcium handling using manganese-enhanced magnetic reson
236 ent with mislocalization of Serca1 and Ryr1, calcium handling was drastically altered in Rbfox1(-/-)
237                                      APD and calcium handling were assessed by live cell imaging with
238 he phosphorylation of substrates involved in calcium handling were disrupted in AKAP5 knockout cardio
239 lar tuft contractility and macula densa cell calcium handling were observed.
240 hearts and isolated cardiomyocytes to assess calcium handling, Western blotting to analyze the involv
241 he endo/sarcoplasmic reticulum with roles in calcium handling, whereas those near AC9 were more abund
242 Overexpression of D1R in CMs disturbs normal calcium handling while CM-specific deletion of D1R ameli
243 weekly prednisone-treated males had improved calcium handling, while comparably treated female muscle
244 ession of genes in the IGF1/PI3K pathway and calcium handling, while female myofibers had profound up
245 ng syncytium with enhanced contractility and calcium handling; while PECs become more mature with sig
246 pha-Tm mutants can be corrected by modifying calcium handling with Parv.
247  liver, we observe an additive impairment in calcium handling without adversely impacting mitochondri

 
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