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1 the deleterious metabolic adaptations of the failing heart.
2 inding protein, is up-regulated in the human failing heart.
3 buting to focal arrhythmia in the intact non-failing heart.
4 a, thereby suppressing FA utilization in the failing heart.
5 e predominant GRK isoform upregulated in the failing heart.
6 FA metabolism and cardiac dysfunction in the failing heart.
7 e A signaling seems to be beneficial for the failing heart.
8 related signaling pathways characterize the failing heart.
9 lopment of novel metabolic therapies for the failing heart.
10 cal therapies as a bridge to recovery of the failing heart.
11 e diastolic stiffness of the healthy and the failing heart.
12 erfusion by enhancing neoangiogenesis in the failing heart.
13 lation of INa by biventricular pacing of the failing heart.
14 ling and preserve cardiac performance in the failing heart.
15 get or affect the ANS and its effects on the failing heart.
16 es maladaptation of energy substrates in the failing heart.
17 duce arrhythmogenic cardiac alternans in the failing heart.
18 olites, and metabolic flux in the normal and failing heart.
19 of caPI3K vector can improve function of the failing heart.
20 susceptible to sustained VF as the untreated failing heart.
21 dent of exercise can restore function of the failing heart.
22 athological mechanism for this kinase in the failing heart.
23 tive stress increases PDE5 expression in the failing heart.
24 OGT (cmOGT KO) and ascertain its role in the failing heart.
25 tween metabolism and cardiac function in the failing heart.
26 ic conditions associated with the normal and failing heart.
27 lication and depletion of mtDNA in the human failing heart.
28 dependent pathology in the hypertrophied and failing heart.
29 ume occurred with increased afterload in the failing heart.
30 athy and severe CHF improves function of the failing heart.
31 d to diseased heart tissue and symptoms of a failing heart.
32 d hormone (T3) that develops in the advanced failing heart.
33 contribute to their beneficial effect on the failing heart.
34 by reactive oxygen species generated in the failing heart.
35 ent, would increase function of the actively failing heart.
36 lyl cyclase VI increases the function of the failing heart.
37 rate metabolism and function in the advanced failing heart.
38 s adenosine may act to inhibit MVO(2) in the failing heart.
39 i) signalling in the normal and mechanically failing heart.
40 nical implications for the management of the failing heart.
41 e myocardial performance in the ischemic and failing heart.
42 SCs) is an emerging therapy for treating the failing heart.
43 stabilizing myocardial NAD(+) levels in the failing heart.
44 red SSB is observed in cardiomyocytes of the failing heart.
45 significantly increases the function of the failing heart.
46 Mg29 to model this observed induction in the failing heart.
47 isms regulating homeostasis of NAD(+) in the failing heart.
48 ping new Ca(2+) buffering strategies for the failing heart.
49 downregulated in myocardial samples from the failing heart.
50 D maps show areas of conduction block in the failing heart.
51 ratures are appropriate for the resuscitated failing heart.
52 TPase (SERCA2a) activity is deficient in the failing heart.
53 ng initiated wave reentry and breakup in the failing heart.
54 gnaling within cardiomyocytes develop in the failing heart.
55 he dysfunctional substrate metabolism of the failing heart.
56 nans is significantly more pronounced in the failing heart.
57 NAD(+) ratio) and protein acetylation in the failing heart.
58 latory system occur in the hypertrophied and failing heart.
59 refore, PKG1alpha activation can benefit the failing heart.
60 shortened action potential duration only in failing hearts.
61 EHDs associate with Cx43 in human and murine failing hearts.
62 tor and inotropic response were decreased in failing hearts.
63 ization when comparing untreated and treated failing hearts.
64 also observed in biopsies derived from human failing hearts.
65 channel trafficking that is downregulated in failing hearts.
66 t altered in left ventricular hypertrophy or failing hearts.
67 egulation of heme and non-heme iron in human failing hearts.
68 PDE4B protein was decreased in human failing hearts.
69 ignificantly less (P=0.011) by almost 80% in failing hearts.
70 phorylated, resulting in "leaky" channels in failing hearts.
71 equally effective in myocytes from normal or failing hearts.
72 evels are maintained above baseline in human failing hearts.
73 bition of RyR2 channels from sheep and human failing hearts.
74 phate (cGMP) signaling is characteristic for failing hearts.
75 similar in LV and BiV pacing, especially in failing hearts.
76 fraction from 42+/-12 to 3+/-2 (P=0.005) in failing hearts.
77 d by comparing B-treated with drug-untreated failing hearts.
78 rected at improving myocardial energetics in failing hearts.
79 activation improves contractile function in failing hearts.
80 also found reduced SIRT6 expression in human failing hearts.
81 sequencing in 70 human control and end-stage failing hearts.
82 cytes contributed to the upregulation in the failing hearts.
83 ications of this finding are investigated in failing hearts.
84 vation might improve contractile function in failing hearts.
85 ed a moderate increase in RV trabeculae from failing hearts.
86 aracteristics resembling those isolated from failing hearts.
87 l for SAN conduction, especially in fibrotic failing hearts.
88 mponent slow rise at the subendocardium in 3 failing hearts.
89 han the subepicardium in both nonfailing and failing hearts.
90 on of SERCA2a itself were greatly reduced in failing hearts.
91 stream gene expression were unchanged in the failing hearts.
92 s PGC-1alpha protein increased by 58% in the failing hearts.
93 quitin proteasome system activity in HCM and failing hearts.
94 associated with the loss of positive FFR in failing hearts.
95 oxidative damage was increased by 50% in the failing hearts.
96 rocess of mtDNA, was decreased by 75% in the failing hearts.
97 or of cardiac hypertrophy, is inactivated in failing hearts.
98 in expression implicated in human and animal failing hearts.
99 ion and size were similar in both normal and failing hearts.
100 ression is downregulated in human and animal failing hearts.
101 een implicated in the aberrant Ca-cycling of failing hearts.
102 or lipoxygenases attenuated mPTP opening in failing hearts.
103 of JMCs underlies contractile dysfunction in failing hearts.
104 significantly upregulated in mouse and human failing hearts.
105 deltac-dependent arrhythmogenic disorders in failing hearts.
106 tion of Ca cycling by protecting stressed or failing hearts.
107 l JMC protein SPEG is downregulated in human failing hearts.
108 uclear-1 were substantially downregulated in failing hearts.
109 umol/L peroxide exposure and in myocyte from failing hearts.
110 ts an additional layer of gene regulation in failing hearts.
111 of normalizing NADH/NAD(+) imbalance in the failing hearts.
112 pic slices isolated from donor and end-stage failing hearts.
113 been shown to provide functional support to failing hearts.
114 icular wedge preparations of human donor and failing hearts.
116 (2) alterations in ketone metabolism in the failing heart, (3) effects of therapeutic ketosis in ani
118 ectrically stimulated myocytes from ischemic failing hearts, AdMYH6 increased the contractile amplitu
119 ement of left ventricular dysfunction in the failing heart after myocardial infarction or doxorubicin
120 ence in regional work between nonfailing and failing hearts after MI and offer novel insight into the
121 P2 in cardiomyocytes facilitated recovery of failing hearts after reversible transverse aortic constr
122 (mtDNA) content was decreased by >40% in the failing hearts, after normalization for a moderate decre
123 onverting enzyme (ACE) is upregulated in the failing heart and has been associated with disease progr
124 een insights into the pathophysiology of the failing heart and illuminate a previously unrecognized p
125 of NAD(+) biosynthetic enzymes in the human failing heart and in the heart of a mouse model of dilat
126 n HF, conferring significant toxicity to the failing heart and markedly increasing its morbidity and
127 e immune-mediated injurious responses in the failing heart and retain this memory on adoptive transfe
128 clude the hemodynamic cross-talk between the failing heart and the response of the kidneys and vice v
131 d the increased abundance of c-kit+ cells in failing hearts and demonstrated frequent coexpression of
133 and succinate decreased from non-failing to failing hearts and did not change significantly post-LVA
134 ic amino acids decreased from non-failing to failing hearts and did not change significantly post-LVA
135 te values both decreased from non-failing to failing hearts and increased again significantly in the
136 cause mitochondrial function is depressed in failing hearts and iron accumulation can lead to oxidati
137 PDE5 is upregulated in hypertrophied and failing hearts and is thought to contribute to their pat
138 ion was decreased in end-stage human DCM and failing hearts and, most importantly, a significant incr
139 ll O-GlcNAc in donor, 68 +/- 9% in end-stage failing heart, and 76 +/- 6% in myectomy muscle samples
140 ged AP duration exclusively in myocytes from failing heart, and the critical conductance required for
141 utophagy may be an adaptive mechanism in the failing heart, and this phenomenon is attenuated by LVAD
142 rdial effects of dyssynchrony and CRT in the failing heart, and we highlight new research aiming to b
145 n is up-regulated in human hypertrophied and failing hearts, and its inhibition (e.g., by sildenafil)
146 in human nonfailing donor hearts, explanted failing hearts, and myectomy samples from patients with
147 n expression was down-regulated in end-stage failing hearts, and that this effect was reverted upon m
148 dyssynchrony is induced by RBBB than LBBB in failing hearts, and the corresponding impact of CRT on t
149 Th1) and Th17 (versus Treg) predominance in failing hearts, and with expansion of memory T cells in
151 er abnormal calcium-handling proteins in the failing heart are candidates for gene therapy; many shor
152 rial dysfunction and energy depletion in the failing heart are innovative therapeutic targets in hear
153 he main features of VF dynamics in a treated failing heart are not affected by the level of electrica
154 molecular and biochemical ECM alterations in failing hearts are dependent on the type of underlying i
155 hondrial function, also are present in human failing hearts as well as in mouse hearts with pathologi
157 2 cm/s (95% CI, 27-37; P=0.001) in 12 native failing hearts at 1000 ms pacing cycle length (PCL).
160 stress but is ultimately detrimental in the failing heart because of accrual of cardiomyocyte death.
161 orms might have therapeutic potential in the failing heart because they increase the maximal force of
162 ransients duration (CaD) in donor but not in failing hearts, because of desensitization of beta1-adre
164 ally nonuniform alteration of AP duration in failing heart blunted the transmural gradient of repolar
165 reased conduction velocity in both donor and failing hearts but shortened action potential duration o
166 e altered Ca(2+) regulatory phenotype of the failing heart, but PKA-mediated phosphorylation of RyRS2
167 bioenergetics is a prominent feature of the failing heart, but the underlying metabolic perturbation
168 ated to glucose metabolism are diminished in failing hearts, but recovered their values post-LVAD.
170 stable increased expression of S100A1 in the failing heart can be used for long-term reversal of LV d
174 sed to increase cardiac contractility of the failing heart center on increasing the amount of calcium
175 This pattern of remodeling was attenuated in failing hearts chronically unloaded with a left ventricu
178 nsient duration was significantly smaller in failing hearts compared with nonfailing hearts at fast p
179 d protein levels (~1.5-2.5-fold increase) in failing hearts compared with nonfailing hearts using our
183 derstand why MyBP-C dephosphorylation in the failing heart contributes to contractile dysfunction and
184 reductions in gap junction coupling occur in failing hearts, contributing to ventricular arrhythmias
186 cycle length decreases, both the normal and failing heart develop T-wave alternans, but only the fai
187 se 4 (HDAC4), upregulation of ANP and BNP in failing hearts did not require increased histone acetyla
191 been observed experimentally that cells from failing hearts exhibit elevated levels of reactive oxyge
194 ar wedge preparations from 6 human end-stage failing hearts (F) and 6 donor hearts rejected for trans
195 et out to measure cardiac metabolites in non-failing hearts, failing hearts, and hearts post-LVAD sup
196 mitochondrial membrane are reviewed for the failing heart from the perspectives of chronic pressure
198 ge amylin oligomers, fibrils, and plaques in failing hearts from obese and diabetic patients but not
199 t studies also identified amylin deposits in failing hearts from patients with obesity or type 2 diab
205 ocaine autoradiography to determine that the failing heart has 30% lower SCN5A levels - the first evi
210 amage and DDR activation are observed in the failing heart, however, the type of DNA damage and its r
211 in vivo gene transfer of AAV9.SERCA2a in the failing heart improved left ventricular contractile func
217 e several components of the phenotype of the failing heart, including contractile function, interstit
218 The overexpression of cTnI-ND in Gsalpha-DF failing hearts increased relaxation velocity and left ve
219 nnels arachidonic acid into EETs, whereas in failing hearts, increased iPLA2gamma activity channels A
220 s of contractile reserve in the stressed and failing heart, inhibition of overactive GRKs has been pr
221 bservations provide direct evidence that the failing heart is "energy starved" as it relates to CK.
222 stolic function, the question of whether the failing heart is "energy starved" has been debated for d
225 The deficit in ATP supplied by CK in the failing heart is cardiac-specific and potentially of suf
231 nce of GRK5 up-regulation in the injured and failing heart is the induction of NF-kappaB expression a
232 hallmark of cells and tissues isolated from failing hearts is prolongation of action potential durat
233 actile performance in human and experimental failing hearts, is impaired calcium sequestration into t
235 To develop therapies aimed at rescuing the failing heart, it is important to understand the molecul
236 of myocardial creatine are a hallmark of the failing heart, leading to the widely held view that crea
237 turnover is reduced in pressure-overloaded, failing hearts, limiting the availability of this rich s
238 (GRKs), some of which are upregulated in the failing heart, making them desirable therapeutic targets
240 that the downregulation of PDE3A observed in failing hearts may play a causative role in the progress
241 rotein were decreased significantly in human failing hearts (n=10) compared with normal hearts (n=3;
243 data show that SERCA2a gene transfer in the failing heart not only improves contractile function but
244 implant) and 8 post-LVAD hearts, plus 8 non-failing hearts obtained from the tissue bank at the Univ
245 a 30% loss in levels of NAD(+) in the murine failing heart of both DCM and transverse aorta constrict
248 s, but not mRNAs or miRNAs, can discriminate failing hearts of different pathologies and are markedly
249 e first demonstration of reduced acyl CoA in failing hearts of humans and mice, and suggests possible
250 444 mRNAs that were altered by >1.3-fold in failing hearts, only 29 mRNAs normalized by as much as 2
251 transcriptional pathways are dysregulated in failing hearts, only recently has the idea of disrupting
253 ially restored after mechanical unloading in failing hearts (P<0.01) and was significantly lower in H
256 he pathophysiological progression of HF, the failing heart reduces fatty acid and glucose oxidation,
257 ing in cardiomyocytes from hypertrophied and failing hearts, reflected as increased diastolic Ca(2+)
259 Accumulating evidence suggests that the failing heart reprograms fuel metabolism toward increase
261 d and phospholamban is hypophosphorylated in failing hearts, resulting in impaired SR Ca2+ reuptake t
263 the cell and tissue level have increased the failing heart's susceptibility to dynamic instabilities
264 ked to metabolic remodelling and whether the failing heart shares a common Na-mediated metabolic 'fin
265 results indicate that the hypertrophied and failing heart shifts to ketone bodies as a significant f
266 trometry revealed that the hypertrophied and failing heart shifts to oxidizing ketone bodies as a fue
268 heart develop T-wave alternans, but only the failing heart shows QRS alternans (although moderate) at
269 to exert profound beneficial effects in the failing heart, suggesting a significant role for PDE5 in
270 repair and antioxidant genes were reduced in failing hearts, suggestive of a defective repair and pro
271 he pattern of metabolite derangements in the failing heart suggests bottlenecks of carbon substrate f
272 c remodeling common to both hypertrophic and failing hearts that are indicative of extracellular matr
274 g function of the postinfarction chronically failing heart, there was late-phase arrhythmogenicity sp
276 n targeting mitochondrial dysfunction in the failing heart to revive the myocardium and its contracti
278 reased betaARK1-coupled PI3K activity in the failing hearts was associated with downregulation of bet
279 achidonic acid (AA) in mitochondria from non-failing hearts was calcium-dependent phospholipase A2zet
280 ble alterations of NAD(+) homeostasis in the failing heart, we quantified the expression of NAD(+) bi
281 junctin levels are severely reduced in human failing hearts, we performed an in-depth study of the me
282 METHODS AND Leukocytes infiltrating the failing heart were analyzed by a multistep enzymatic pro
284 Ca(2+) cycling perturbations manifest in the failing heart, where their protein levels are significan
285 ase termination was changed in myocytes from failing hearts, where remodelling processes lead to alte
286 The need for mechanical assistance of the failing heart, whether acute after a myocardial infarcti
287 ently reported reduced OGA expression in the failing heart, which is consistent with the pro-adaptive
288 ft ventricular hypertrophy, but decreased in failing hearts, while ryanodine receptor was unchanged i
290 f cardiac resynchronization therapy (CRT) in failing hearts with a pure right (RBBB) versus left bund
292 ronization therapy is effective for treating failing hearts with conduction delay and discoordinate c
294 ignificantly changed in the hypertrophied or failing heart, with the notable exception of a progressi
295 ver the roles of cardiac titin in normal and failing hearts, with a special emphasis on the contribut
296 idates are often differentially expressed in failing hearts, with an inverse correlation between 3'UT
297 ved a significant increase in heme levels in failing hearts, with corresponding feedback inhibition o
298 ea of LV lateral wall in both nonfailing and failing hearts, with modest anterior or posterior deviat