ライフサイエンスコーパス: myocardial remodeling

1 timulating neovascularization, and promoting myocardial remodeling.

2 -induced changes in cardiac metabolism cause myocardial remodeling.

3 development, supporting a concept of global myocardial remodeling.

4 al homeostasis and the prevention of adverse myocardial remodeling.

5 e overload, suggesting its important role in myocardial remodeling.

6 % male), and 20 hypertensives with prominent myocardial remodeling.

7 ecies, which may be important when examining myocardial remodeling.

8 eroxic challenge during reoxygenation causes myocardial remodeling.

9 aneurysm, collateral vessel development and myocardial remodeling.

10 enal function and may simultaneously inhibit myocardial remodeling.

11 se onset on cardiomyocyte death and fibrotic myocardial remodeling.

12 ad, and dilated cardiomyopathy) that involve myocardial remodeling.

13 f gene expression plays an important role in myocardial remodeling.

14 ve demonstrated a role for MMP activation in myocardial remodeling.

15 hich would potentially enhance extracellular myocardial remodeling.

16 ciated with left ventricle (LV) dilation and myocardial remodeling.

17 ated with left ventricular (LV) dilation and myocardial remodeling.

18 tial intracellular mechanism for postinfarct myocardial remodeling.

19 that mitochondrial processes participate in myocardial remodeling after infarction.

20 t likely a result of favorable effects on LV myocardial remodeling and contractile processes.

21 , NAFLD remained associated with subclinical myocardial remodeling and dysfunction (P < 0.01).

22 lin D2-induced cardiomyocyte renewal reduced myocardial remodeling and dysfunction after pressure ove

23 is independently associated with subclinical myocardial remodeling and dysfunction and provides furth

24 Myocardial remodeling and dysfunction are serious compli

25 calpain-1 and calpain-2 activities, reduces myocardial remodeling and dysfunction following MI, and

26 ent mechanism of serotonin may contribute to myocardial remodeling and failure.

27 implicated in the pathophysiology of chronic myocardial remodeling and failure.

28 for oxidative stress in the pathogenesis of myocardial remodeling and failure.

29 ro, possess distinct properties, and improve myocardial remodeling and function in experimental model

30 otentially effective approach to reverse the myocardial remodeling and heart failure processes, parti

31 the heart and its physiological relevance in myocardial remodeling and heart failure remain largely u

32 mulation has been implicated in pathological myocardial remodeling and heart failure.

33 ill also open new perspectives in evaluating myocardial remodeling and in assessing the kinetics of s

34 merges as a crucial mediator of postischemic myocardial remodeling and may evolve as a novel pharmaco

35 clusion, deficiency of Capn4 reduces adverse myocardial remodeling and myocardial dysfunction after M

36 ons suggest the involvement of HIF-1alpha in myocardial remodeling and peri-infarct vascularization.

37 roRNAs play critical regulatory roles during myocardial remodeling and progression to heart failure.

38 one (NP12), lessens the magnitude of adverse myocardial remodeling and promotes angiogenesis.

39 and constitutes a novel mechanism underlying myocardial remodeling and sudden cardiac death.

40 aling cascade that is linked to pathological myocardial remodeling and to regulation of key proteins

41 s the ability to reverse already-established myocardial remodeling and ventricular dysfunction, with

42 r a period of 7 months to evaluate survival, myocardial remodeling, and function by echocardiography

43 k7) in regulating necroptotic myocyte death, myocardial remodeling, and heart failure propensity.

44 y of ginseng to reverse cardiac hypertrophy, myocardial remodeling, and heart failure, which was asso

45 inflammation, and reversal of sepsis-induced myocardial remodeling are likely to underlie its benefic

46 identifying it as a potential biomarker for myocardial remodeling assessment in HCM.

47 MMP inhibition significantly attenuates the myocardial remodeling associated with chronic volume ove

48 ssociated with the severity of LA fibrofatty myocardial remodeling at histologic analysis.

49 , PKCepsilon may negatively regulate adverse myocardial remodeling by cooperating with CN to downregu

50 To discern altered control of myocardial remodeling by PKG, HFPEF was compared with ao

51 nd fibrotic genes known to be influential in myocardial remodeling changed as a result of TSP-4 defic

52 Myocardial remodeling driven by excess pressure and volu

53 Neutrophils are thought to orchestrate myocardial remodeling during the early progression to ca

54 lay a key role in collagen deposition during myocardial remodeling following MI by modulating cytokin

55 sal relationship between calpain and post-MI myocardial remodeling has not been fully understood.

56 es a severe pathologic phenotype composed of myocardial remodeling, heart failure, and pronounced mor

57 furthering our understanding of the role of myocardial remodeling in cardiovascular disease.

58 e matrix metalloproteinases (MMPs) can cause myocardial remodeling in chronic disease states, but how

59 Together, these proteins may contribute to myocardial remodeling in congestive heart failure.

60 ed myocardial MMP activity contributes to LV myocardial remodeling in developing CHF.

61 o ZDV and CHDs, and a long-lasting postnatal myocardial remodeling in girls.

62 Prominent features of myocardial remodeling in heart failure with preserved ej

63 Myocardial remodeling in HFPEF differs from heart failur

64 ar functional recovery and the prevention of myocardial remodeling in Kit(+/+) mice, which was elimin

65 Here, we examine the role of adiponectin in myocardial remodeling in response to acute injury.

66 d-type (WT) littermates were used to compare myocardial remodeling in response to isoproterenol (Iso)

67 MMP/TIMP stoichiometry that would facilitate myocardial remodeling in the early post-MI setting.

68 The temporal myocardial remodeling induced by chronic ventricular vol

69 Increased myocardial remodeling, inflammation, and volume overload

70 Myocardial remodeling is a complex process involving sev

71 LV myocardial remodeling is a structural hallmark of hypert

72 There is now widespread recognition that myocardial remodeling is an important driving force behi

73 lood, a process of ischemia, infarction, and myocardial remodeling is initiated.

74 tissue regeneration, but their mechanism for myocardial remodeling is still unclear.

75 tissue regeneration, but their mechanism for myocardial remodeling is still unclear.

76 sion may be a fundamental feature of adverse myocardial remodeling, it appears to be treatable, and i

77 gardless of insult, can trigger compensatory myocardial remodeling leading to heart failure.

78 hly selective approach for targeting adverse myocardial remodeling linked to betaAR signaling.

79 is independently associated with subclinical myocardial remodeling or dysfunction among the general p

80 the timing of sMMPi and regional and global myocardial remodeling patterns after MI.

81 tudies on this dynamic entity and on adverse myocardial remodeling that have been published over the

82 was to evaluate interstitial alterations in myocardial remodeling using a radiolabeled Cy5.5-RGD ima

83 Myocardial remodeling was accompanied by beneficial chan

84 rmine whether microRNAs (miRNAs) involved in myocardial remodeling were differentially expressed in t

85 resulted in cardiomyopathy characterized by myocardial remodeling with interstitial fibrosis, with r

86 alloproteinases (MMPs) contribute to adverse myocardial remodeling with ischemia and reperfusion.