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1 ys a central role in disease progression and myocardial remodeling.
2 0.05), suggesting that anemia contributes to myocardial remodeling.
3 ex-specific pathways linking stress to early myocardial remodeling.
4 timulating neovascularization, and promoting myocardial remodeling.
5 -induced changes in cardiac metabolism cause myocardial remodeling.
6 % male), and 20 hypertensives with prominent myocardial remodeling.
7 respond to cardiac injury and participate in myocardial remodeling.
8 se onset on cardiomyocyte death and fibrotic myocardial remodeling.
9  development, supporting a concept of global myocardial remodeling.
10 al homeostasis and the prevention of adverse myocardial remodeling.
11 e overload, suggesting its important role in myocardial remodeling.
12 ecies, which may be important when examining myocardial remodeling.
13 eroxic challenge during reoxygenation causes myocardial remodeling.
14  aneurysm, collateral vessel development and myocardial remodeling.
15 enal function and may simultaneously inhibit myocardial remodeling.
16 ad, and dilated cardiomyopathy) that involve myocardial remodeling.
17 f gene expression plays an important role in myocardial remodeling.
18 ve demonstrated a role for MMP activation in myocardial remodeling.
19 hich would potentially enhance extracellular myocardial remodeling.
20 ciated with left ventricle (LV) dilation and myocardial remodeling.
21 ated with left ventricular (LV) dilation and myocardial remodeling.
22 tial intracellular mechanism for postinfarct myocardial remodeling.
23  that mitochondrial processes participate in myocardial remodeling after infarction.
24 nd angiotensin receptor blocker valsartan on myocardial remodeling and cardiac perfusion in experimen
25 t likely a result of favorable effects on LV myocardial remodeling and contractile processes.
26 , NAFLD remained associated with subclinical myocardial remodeling and dysfunction (P < 0.01).
27 lin D2-induced cardiomyocyte renewal reduced myocardial remodeling and dysfunction after pressure ove
28 is independently associated with subclinical myocardial remodeling and dysfunction and provides furth
29                                              Myocardial remodeling and dysfunction are serious compli
30  calpain-1 and calpain-2 activities, reduces myocardial remodeling and dysfunction following MI, and
31 hibition of eCyPA prevented (Ang II)-induced myocardial remodeling and dysfunction in mice.
32 ent mechanism of serotonin may contribute to myocardial remodeling and failure.
33 implicated in the pathophysiology of chronic myocardial remodeling and failure.
34  for oxidative stress in the pathogenesis of myocardial remodeling and failure.
35  myocardial infarction (MI), contributing to myocardial remodeling and fibrosis.
36 ro, possess distinct properties, and improve myocardial remodeling and function in experimental model
37 ory cytokine that has deleterious effects in myocardial remodeling and function.
38 otentially effective approach to reverse the myocardial remodeling and heart failure processes, parti
39 the heart and its physiological relevance in myocardial remodeling and heart failure remain largely u
40 mulation has been implicated in pathological myocardial remodeling and heart failure.
41 he importance of managing anemia to mitigate myocardial remodeling and improve clinical outcomes.
42 ill also open new perspectives in evaluating myocardial remodeling and in assessing the kinetics of s
43 merges as a crucial mediator of postischemic myocardial remodeling and may evolve as a novel pharmaco
44 ve and parasympathetic withdrawal exacerbate myocardial remodeling and metabolic dysfunction, both of
45 clusion, deficiency of Capn4 reduces adverse myocardial remodeling and myocardial dysfunction after M
46  Sacubitril/Valsartan Therapy on Biomarkers, Myocardial Remodeling and Outcomes [PROVE-HF]; NCT028871
47 ons suggest the involvement of HIF-1alpha in myocardial remodeling and peri-infarct vascularization.
48 roRNAs play critical regulatory roles during myocardial remodeling and progression to heart failure.
49 one (NP12), lessens the magnitude of adverse myocardial remodeling and promotes angiogenesis.
50 tween relaxin and Wnt-signaling resulting in myocardial remodeling and reveals a fundamental mechanis
51 and constitutes a novel mechanism underlying myocardial remodeling and sudden cardiac death.
52 aling cascade that is linked to pathological myocardial remodeling and to regulation of key proteins
53 s the ability to reverse already-established myocardial remodeling and ventricular dysfunction, with
54 r a period of 7 months to evaluate survival, myocardial remodeling, and function by echocardiography
55 lta is critically involved in the mortality, myocardial remodeling, and heart failure (HF) progressio
56 k7) in regulating necroptotic myocyte death, myocardial remodeling, and heart failure propensity.
57 y of ginseng to reverse cardiac hypertrophy, myocardial remodeling, and heart failure, which was asso
58 ergent effects on left ventricular function, myocardial remodeling, and monocyte recruitment.
59 s study was to examine the clinical profile, myocardial remodeling, and survival of patients with PPC
60 ation in aortic stenosis and their impact on myocardial remodeling, aortic valve flow patterns, and c
61 inflammation, and reversal of sepsis-induced myocardial remodeling are likely to underlie its benefic
62  identifying it as a potential biomarker for myocardial remodeling assessment in HCM.
63  MMP inhibition significantly attenuates the myocardial remodeling associated with chronic volume ove
64 ssociated with the severity of LA fibrofatty myocardial remodeling at histologic analysis.
65 , PKCepsilon may negatively regulate adverse myocardial remodeling by cooperating with CN to downregu
66                To discern altered control of myocardial remodeling by PKG, HFPEF was compared with ao
67 nd fibrotic genes known to be influential in myocardial remodeling changed as a result of TSP-4 defic
68             Often, pressure overload-induced myocardial remodeling does not undergo complete reverse
69                                              Myocardial remodeling driven by excess pressure and volu
70       Neutrophils are thought to orchestrate myocardial remodeling during the early progression to ca
71 lay a key role in collagen deposition during myocardial remodeling following MI by modulating cytokin
72  to evaluate heart function and pathological myocardial remodeling following stress.
73  HCM and that SDB is associated with adverse myocardial remodeling, greater diastolic dysfunction, an
74 sal relationship between calpain and post-MI myocardial remodeling has not been fully understood.
75 es a severe pathologic phenotype composed of myocardial remodeling, heart failure, and pronounced mor
76                                  The role of myocardial remodeling in altering the mechanics of faili
77  furthering our understanding of the role of myocardial remodeling in cardiovascular disease.
78 e matrix metalloproteinases (MMPs) can cause myocardial remodeling in chronic disease states, but how
79   Together, these proteins may contribute to myocardial remodeling in congestive heart failure.
80 ed myocardial MMP activity contributes to LV myocardial remodeling in developing CHF.
81 o ZDV and CHDs, and a long-lasting postnatal myocardial remodeling in girls.
82                        Prominent features of myocardial remodeling in heart failure with preserved ej
83                                              Myocardial remodeling in HFPEF differs from heart failur
84 ar functional recovery and the prevention of myocardial remodeling in Kit(+/+) mice, which was elimin
85  highlighting the pivotal role of elastin in myocardial remodeling in mouse models with deletions of
86 nists were recently shown to protect against myocardial remodeling in preclinical studies and to impr
87  Here, we examine the role of adiponectin in myocardial remodeling in response to acute injury.
88 d-type (WT) littermates were used to compare myocardial remodeling in response to isoproterenol (Iso)
89 ial dynamics and function and contributes to myocardial remodeling in rodent models of heart failure.
90 MMP/TIMP stoichiometry that would facilitate myocardial remodeling in the early post-MI setting.
91 s and prognosis of cardiac disease involving myocardial remodeling, including myocardial infarction a
92                                 The temporal myocardial remodeling induced by chronic ventricular vol
93                                    Increased myocardial remodeling, inflammation, and volume overload
94                                              Myocardial remodeling is a complex process involving sev
95                                           LV myocardial remodeling is a structural hallmark of hypert
96     There is now widespread recognition that myocardial remodeling is an important driving force behi
97 lood, a process of ischemia, infarction, and myocardial remodeling is initiated.
98 Visualization and quantification of fibrotic myocardial remodeling is one of the greatest assets that
99 tissue regeneration, but their mechanism for myocardial remodeling is still unclear.
100 tissue regeneration, but their mechanism for myocardial remodeling is still unclear.
101 sion may be a fundamental feature of adverse myocardial remodeling, it appears to be treatable, and i
102 gardless of insult, can trigger compensatory myocardial remodeling leading to heart failure.
103 hly selective approach for targeting adverse myocardial remodeling linked to betaAR signaling.
104 is independently associated with subclinical myocardial remodeling or dysfunction among the general p
105  the timing of sMMPi and regional and global myocardial remodeling patterns after MI.
106 lammatory state contributing to vascular and myocardial remodeling processes resulting in atheroscler
107 tudies on this dynamic entity and on adverse myocardial remodeling that have been published over the
108 eals the biological basis for chronic atrial myocardial remodeling that paves the way of atrial fibri
109  was to evaluate interstitial alterations in myocardial remodeling using a radiolabeled Cy5.5-RGD ima
110                                              Myocardial remodeling was accompanied by beneficial chan
111 t-induced VO, and the progression of adverse myocardial remodeling was assessed by serial echocardiog
112 rmine whether microRNAs (miRNAs) involved in myocardial remodeling were differentially expressed in t
113  resulted in cardiomyopathy characterized by myocardial remodeling with interstitial fibrosis, with r
114 alloproteinases (MMPs) contribute to adverse myocardial remodeling with ischemia and reperfusion.

 
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