ライフサイエンスコーパス: vasoprotective

1 Estrogens demonstrate vasoprotective activity in many experimental models.

2 rahydrobiopterin (BH4) is a major endogenous vasoprotective agent that improves endothelial function

3 ilability, and employing neuroprotective and vasoprotective agents.

4 ed octapeptides suggesting that their potent vasoprotective and anti-inflammatory activity is not nit

5 These results suggest an interplay between vasoprotective and pro-inflammatory endothelial molecule

6 etin have shown antioxidant, cytoprotective, vasoprotective, antiproliferative and antiinflammatory p

7 Hydrogen sulphide (H2 S) is vasoprotective, attenuates inflammation and modulates bl

8 ects were associated with an increase in the vasoprotective axis of the lung renin-angiotensin system

9 enzyme (ACE)-2 is the primary enzyme of the vasoprotective axis of the renin angiotensin system that

10 sexes, whether (1) exogenous estrogen has a vasoprotective effect in injured carotid arteries, (2) p

11 These results indicate that the vasoprotective effect of E2 in the balloon-injured rat c

12 antagonist, to test the hypothesis that the vasoprotective effect of E2 in the rat carotid injury mo

13 ably by blocking the production and thus the vasoprotective effect of endogenous estrogen.

14 medroxyprogesterone acetate, MPA) blocks the vasoprotective effect of estrogen, and (3) any observed

15 The mechanisms of this vasoprotective effect of female sex are incompletely und

16 The vasoprotective effect of hormone replacement therapy may

17 This vasoprotective effect was independent of enhanced circul

18 lling into question the ER dependency of the vasoprotective effect.

19 gesting that 17beta-estradiol may also exert vasoprotective effects in cerebral blood vessels via sti

20 These results demonstrate that the vasoprotective effects of E(2) after ligation vascular i

21 se, likely because of its attenuation of the vasoprotective effects of endothelial nitric oxide synth

22 The vasoprotective effects of estrogen are age-dependent and

23 The vasoprotective effects of estrogen are mediated by estro

24 Future studies designed to preserve the vasoprotective effects of estrogen in older women are ne

25 tions of ER and is essential for many of the vasoprotective effects of estrogen.

26 eas addition of MPA to estradiol blocked the vasoprotective effects of estrogen.

27 t another potential mechanism underlying the vasoprotective effects of estrogens but also that the es

28 but not intact females are resistant to the vasoprotective effects of exogenous estrogen, despite at

29 The vasoprotective effects of nitrite were counteracted by i

30 of SOCS3 abolished the antiinflammatory and vasoprotective effects of RORalpha deficiency in vitro a

31 The vasoprotective effects of statins in heart transplant re

32 that SRC-3 largely facilitates ER-dependent vasoprotective effects under conditions of vascular trau

33 In vivo vasoprotective effects were determined using: (1) a carr

34 f nitric oxide, may exert vasomodulatory and vasoprotective effects.

35 eptor that primarily underlies CNP-dependent vasoprotective functions and developed small-molecule NP

36 d preservation solution on the expression of vasoprotective genes, and on endothelial activation and

37 Estrogen is vasoprotective in animal models of vascular injury, yet

38 ous studies have shown that estrogen (E2) is vasoprotective in multiple animal models of vascular inj

39 lls isolated from young women but that these vasoprotective mechanisms are lost in women who are aged

40 te that HO-1 represents an important in vivo vasoprotective mediator that is capable of attenuating t

41 , 9.0+/-2.4%), and the rates of use of other vasoprotective medications were low (e.g., 30% of partic

42 Estrogen is an important vasoprotective molecule that causes the rapid dilation o

43 Endothelial thrombomodulin is a major vasoprotective molecule.

44 Prostacyclin is an important vasoprotective molecule.

45 xygen and nitrogen free radicals rather than vasoprotective nitric oxide for unclear reasons.

46 ment blocked the decay of KLF2, sustaining a vasoprotective phenotype, and preventing endothelial act

47 nale to evaluate the beneficial effects of a vasoprotective preservation solution on human liver proc

48 Expression of KLF2 and its vasoprotective programs decrease in HEC incubated under

49 Expression of KLF2 and its vasoprotective programs was determined in (i) hepatic en

50 cold storage conditions disrupts endothelial vasoprotective programs, and that this consequence of st

51 harmacologic agents that restore endothelial vasoprotective programs, by upregulating KLF2, may repre

52 storage solution, maintained KLF2-dependent vasoprotective programs, prevented liver damage, inflamm

53 This study highlights BNP's vasoprotective propensity, bringing to light a possible

54 is a peptide molecule with anti-fibrotic and vasoprotective properties that binds to relaxin family p

55 sidering the fact that nitric oxide exhibits vasoprotective properties, we examined the effects of ni

56 estoring the balance between the classic and vasoprotective renin angiotensin system.

57 Given the central vasoprotective role of endothelium, these findings could

58 Such a novel vasoprotective role of PGRN may contribute to brain dysf

59 rogenitor cells (EPCs) enhance production of vasoprotective substances in cerebral arteries.

60 factor Kruppel-like factor 2 (KLF2) and its vasoprotective target genes were assessed during cold st

61 naling is altered in older women, converting vasoprotective to vasotoxic effects.

62 due to a reduction in the expression of the vasoprotective transcription factor Kruppel-like Factor

63 The expression of endothelial KLF2 and its vasoprotective transcriptional targets were rapidly lost

64 is exposed to various flow patterns such as vasoprotective unidirectional laminar shear stress (LSS)