ライフサイエンスコーパス: mesangial matrix

1 hains (these chains normally localize to the mesangial matrix).

2 nt membrane thickness and a >50% increase in mesangial matrix.

3 angium with diffuse and nodular expansion of mesangial matrix.

4 the renal glomerulus and are surrounded by a mesangial matrix.

5 erate focal tubular atrophy and an increased mesangial matrix.

6 eading to chronic accumulation of glomerular mesangial matrix.

7 ased numbers of mesangial cells and expanded mesangial matrix.

8 vanced glomerular lesions, including diffuse mesangial matrix accumulation and fibrin cap formation.

9 s an important factor in the pathogenesis of mesangial matrix accumulation and progressive glomerulos

10 significantly reduced albuminuria and kidney mesangial matrix accumulation in the db/db mice model in

11 ced albuminuria, glomerular hypertrophy, and mesangial matrix accumulation in the F1 Akita model of D

12 Mesangial matrix accumulation is an early feature of glo

13 b mouse, a model of type 2 diabetes in which mesangial matrix accumulation is evident by 20 wk of age

14 bition of mesangial collagenase activity, 2) mesangial matrix accumulation, and 3) in-crease in trans

15 its, mesangial cell proliferation, extensive mesangial matrix accumulation, and macrophage influx.

16 with DKD, including glomerular hypertrophy, mesangial matrix accumulation, glomerular basement membr

17 the regulation of renal blood flow, GFR, and mesangial matrix accumulation.

18 cumulation of electron-dense material in the mesangial matrix and age-dependent formation of intrames

19 for involvement in the restructuring of the mesangial matrix and in the migration of MC in disease.

20 integrin alpha1 expression, expansion of the mesangial matrix and podocyte foot process effacement ar

21 Perlecan is the major HSPG of mesangial matrix and subendothelial space, and consisten

22 There was also increased mesangial matrix and thickening of the glomerular and tu

23 of mice studied after 8 months of diabetes, mesangial matrix area, calculated as a fraction of total

24 Glomerular hypertrophy and accumulation of mesangial matrix, characteristic of early DN, were prese

25 ism controlling the accumulation of specific mesangial matrix components.

26 ngial cells, and they suggest that decreased mesangial matrix degradation, caused by TGF-beta-mediate

27 Because the PIP complex promotes glomerular mesangial matrix deposition and protects podocytes from

28 important in the pathogenesis of the excess mesangial matrix deposition of diabetic and other glomer

29 einuria, lowered collagen IV deposits in the mesangial matrix, diminished mesangial matrix expansion

30 associated with renal damage, in particular mesangial matrix expansion (MME).

31 PFD treatment significantly reduced mesangial matrix expansion and expression of renal matri

32 deposits in the mesangial matrix, diminished mesangial matrix expansion and extended lifespan.

33 ks of age reduced 24-h albumin excretion and mesangial matrix expansion and improved glomerular ultra

34 etic mice decreased albuminuria and improved mesangial matrix expansion and podocyte morphology.

35 Untreated db/db mice developed mesangial matrix expansion and tubular epithelial cell a

36 minuria, renal insufficiency, and glomerular mesangial matrix expansion associated with increased ren

37 b mice developed progressive albuminuria and mesangial matrix expansion between weeks 20 and 22, asso

38 sults suggest that ILK is likely involved in mesangial matrix expansion in response to hyperglycemia

39 ce failed to develop significantly increased mesangial matrix expansion or thickening of the glomerul

40 as lead classifier genes in relation to the mesangial matrix expansion phenotype.

41 ed in the SU5416-treated db/db mice, whereas mesangial matrix expansion remained unchanged by treatme

42 Albuminuria, mesangial matrix expansion, and glomerular hypertrophy w

43 factor beta, renal insufficiency, glomerular mesangial matrix expansion, and glomerulosclerosis in as

44 albuminuria, glomerular basement thickening, mesangial matrix expansion, and hypertension, compared w

45 associated with reduction in proteinuria and mesangial matrix expansion, and prevention of the overex

46 events the development of renal hypertrophy, mesangial matrix expansion, and the decline in renal fun

47 ormalities such as focal glomerulosclerosis, mesangial matrix expansion, and thickening of basement m

48 tions of type I diabetic nephropathy include mesangial matrix expansion, basement membrane thickening

49 reduced whole kidney glomerular hypertrophy, mesangial matrix expansion, extracellular matrix accumul

50 netic model of type 2 diabetes that exhibits mesangial matrix expansion, glomerular basement membrane

51 diabetic nephropathy with microalbuminuria, mesangial matrix expansion, glomerular basement membrane

52 tic Fcgamma receptor-deficient mice had less mesangial matrix expansion, inflammatory cell infiltrati

53 al insufficiency with arteriolar hyalinosis, mesangial matrix expansion, mesangiolysis with microaneu

54 n near-complete reversal of both structural (mesangial matrix expansion, mesangiolysis, basement memb

55 samples based on the presence or absence of mesangial matrix expansion, the best indicator for the d

56 transforming growth factor beta, glomerular mesangial matrix expansion, the extent of glomeruloscler

57 n seems to play a key role in the subsequent mesangial matrix expansion, we tested the response of cu

58 ed albuminuria, foot-process effacement, and mesangial matrix expansion.

59 etion, glomerular and renal hypertrophy, and mesangial matrix expansion.

60 angial deposition of vWF was associated with mesangial matrix expansion.

61 n a significant reduction of albuminuria and mesangial matrix expansion.

62 l mediator of diabetic renal hypertrophy and mesangial matrix expansion.

63 ean +/- SD 0.30 +/- 0.06 vs. 0.27 +/- 0.07), mesangial matrix fractional volume (0.16 +/- 0.05 vs. 0.

64 olume (0.16 +/- 0.05 vs. 0.16 +/- 0.06), and mesangial matrix fractional volume per total mesangium (

65 Similarly, apoE induced the mesangial matrix HSPG.

66 y creatinine clearance, and the expansion of mesangial matrix in db/db mice.

67 Accumulation of mesangial matrix in diabetic nephropathy is caused by in

68 f FGFR and FGF-1, which was localized to the mesangial matrix in glomeruli from normal human kidneys.

69 tigate mechanisms underlying accumulation of mesangial matrix in OVE26 mice.

70 is and tubular atrophy (IFTA), 4.8% abnormal mesangial matrix increase, 32.0% abnormal arteriolar hya

71 of anionic HSPG in the basement membrane and mesangial matrix is associated with disruption of filtra

72 ar mesangial cells (HMC) are embedded in the mesangial matrix (MM) and control its turnover through a

73 betic nephropathy characterized by increased mesangial matrix protein (e.g., collagen) accumulation.

74 pathway responsible for HG-induced increased mesangial matrix synthesis, a hallmark of diabetic nephr

75 PAI-1 appears to reduce glomerular mesangial matrix turnover by inhibiting plasminogen acti

76 versus 1.33 +/- 0.39 x 10(6) microm(3)), and mesangial matrix volume per glomerulus (0.15 +/- 0.05 ve

77 eta, collagen alpha1(IV), nitrotyrosine, and mesangial matrix were all significantly increased compar