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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 reases in albuminuria, urinary H(2)O(2), and mesangial matrix accumulation in db/db mice and fully pr
11 significantly reduced albuminuria and kidney mesangial matrix accumulation in the db/db mice model in
12 ced albuminuria, glomerular hypertrophy, and mesangial matrix accumulation in the F1 Akita model of D
13                                              Mesangial matrix accumulation is an early feature of glo
14 b mouse, a model of type 2 diabetes in which mesangial matrix accumulation is evident by 20 wk of age
15 bition of mesangial collagenase activity, 2) mesangial matrix accumulation, and 3) in-crease in trans
16 its, mesangial cell proliferation, extensive mesangial matrix accumulation, and macrophage influx.
17 dation, and increased levels of albuminuria, mesangial matrix accumulation, and urinary H(2)O(2) Admi
18  with DKD, including glomerular hypertrophy, mesangial matrix accumulation, glomerular basement membr
19 the regulation of renal blood flow, GFR, and mesangial matrix accumulation.
20 cumulation of electron-dense material in the mesangial matrix and age-dependent formation of intrames
21 e and histologically scored them for percent mesangial matrix and glomerular volume (~50 glomeruli pe
22  for involvement in the restructuring of the mesangial matrix and in the migration of MC in disease.
23 integrin alpha1 expression, expansion of the mesangial matrix and podocyte foot process effacement ar
24                Perlecan is the major HSPG of mesangial matrix and subendothelial space, and consisten
25                     There was also increased mesangial matrix and thickening of the glomerular and tu
26  of mice studied after 8 months of diabetes, mesangial matrix area, calculated as a fraction of total
27   Glomerular hypertrophy and accumulation of mesangial matrix, characteristic of early DN, were prese
28 ism controlling the accumulation of specific mesangial matrix components.
29 ngial cells, and they suggest that decreased mesangial matrix degradation, caused by TGF-beta-mediate
30  Because the PIP complex promotes glomerular mesangial matrix deposition and protects podocytes from
31 ced albuminuria, glomerular hypertrophy, and mesangial matrix deposition in streptozotocin (STZ)-indu
32  important in the pathogenesis of the excess mesangial matrix deposition of diabetic and other glomer
33 einuria, lowered collagen IV deposits in the mesangial matrix, diminished mesangial matrix expansion
34  associated with renal damage, in particular mesangial matrix expansion (MME).
35 lso accompanied by histologic kidney injury (mesangial matrix expansion and apoptosis).
36          PFD treatment significantly reduced mesangial matrix expansion and expression of renal matri
37 deposits in the mesangial matrix, diminished mesangial matrix expansion and extended lifespan.
38 ks of age reduced 24-h albumin excretion and mesangial matrix expansion and improved glomerular ultra
39 etic mice decreased albuminuria and improved mesangial matrix expansion and podocyte morphology.
40               Untreated db/db mice developed mesangial matrix expansion and tubular epithelial cell a
41 minuria, renal insufficiency, and glomerular mesangial matrix expansion associated with increased ren
42 b mice developed progressive albuminuria and mesangial matrix expansion between weeks 20 and 22, asso
43 sults suggest that ILK is likely involved in mesangial matrix expansion in response to hyperglycemia
44 ce failed to develop significantly increased mesangial matrix expansion or thickening of the glomerul
45  as lead classifier genes in relation to the mesangial matrix expansion phenotype.
46 ed in the SU5416-treated db/db mice, whereas mesangial matrix expansion remained unchanged by treatme
47 notype classifications highly correlate with mesangial matrix expansion scored by a pathologist (R.E.
48 logic analysis of glomerular hypertrophy and mesangial matrix expansion were also used to assess DN i
49                                 Albuminuria, mesangial matrix expansion, and glomerular hypertrophy w
50 factor beta, renal insufficiency, glomerular mesangial matrix expansion, and glomerulosclerosis in as
51 albuminuria, glomerular basement thickening, mesangial matrix expansion, and hypertension, compared w
52 associated with reduction in proteinuria and mesangial matrix expansion, and prevention of the overex
53 events the development of renal hypertrophy, mesangial matrix expansion, and the decline in renal fun
54 ormalities such as focal glomerulosclerosis, mesangial matrix expansion, and thickening of basement m
55 ssive renal pathologies, including fibrosis, mesangial matrix expansion, and tubular hypertrophy were
56 tions of type I diabetic nephropathy include mesangial matrix expansion, basement membrane thickening
57 reduced whole kidney glomerular hypertrophy, mesangial matrix expansion, extracellular matrix accumul
58  diabetic nephropathy with microalbuminuria, mesangial matrix expansion, glomerular basement membrane
59 netic model of type 2 diabetes that exhibits mesangial matrix expansion, glomerular basement membrane
60 tic Fcgamma receptor-deficient mice had less mesangial matrix expansion, inflammatory cell infiltrati
61 al insufficiency with arteriolar hyalinosis, mesangial matrix expansion, mesangiolysis with microaneu
62 n near-complete reversal of both structural (mesangial matrix expansion, mesangiolysis, basement memb
63  samples based on the presence or absence of mesangial matrix expansion, the best indicator for the d
64  transforming growth factor beta, glomerular mesangial matrix expansion, the extent of glomeruloscler
65 njuries, exhibiting more severe albuminuria, mesangial matrix expansion, tubulointerstitial lesions,
66 n seems to play a key role in the subsequent mesangial matrix expansion, we tested the response of cu
67 ed albuminuria, foot-process effacement, and mesangial matrix expansion.
68 etion, glomerular and renal hypertrophy, and mesangial matrix expansion.
69 angial deposition of vWF was associated with mesangial matrix expansion.
70 n a significant reduction of albuminuria and mesangial matrix expansion.
71 l mediator of diabetic renal hypertrophy and mesangial matrix expansion.
72 ean +/- SD 0.30 +/- 0.06 vs. 0.27 +/- 0.07), mesangial matrix fractional volume (0.16 +/- 0.05 vs. 0.
73 olume (0.16 +/- 0.05 vs. 0.16 +/- 0.06), and mesangial matrix fractional volume per total mesangium (
74 osome 7, with a peak at ~30 Mbp, for percent mesangial matrix, glomerular volume, and mesangial volum
75                  Similarly, apoE induced the mesangial matrix HSPG.
76 y creatinine clearance, and the expansion of mesangial matrix in db/db mice.
77                              Accumulation of mesangial matrix in diabetic nephropathy is caused by in
78 f FGFR and FGF-1, which was localized to the mesangial matrix in glomeruli from normal human kidneys.
79 tigate mechanisms underlying accumulation of mesangial matrix in OVE26 mice.
80 is and tubular atrophy (IFTA), 4.8% abnormal mesangial matrix increase, 32.0% abnormal arteriolar hya
81 of anionic HSPG in the basement membrane and mesangial matrix is associated with disruption of filtra
82 ar mesangial cells (HMC) are embedded in the mesangial matrix (MM) and control its turnover through a
83 ockout mice exhibited a mild increase of the mesangial matrix, moderate thickening of the glomerular
84 betic nephropathy characterized by increased mesangial matrix protein (e.g., collagen) accumulation.
85 pathway responsible for HG-induced increased mesangial matrix synthesis, a hallmark of diabetic nephr
86           PAI-1 appears to reduce glomerular mesangial matrix turnover by inhibiting plasminogen acti
87 versus 1.33 +/- 0.39 x 10(6) microm(3)), and mesangial matrix volume per glomerulus (0.15 +/- 0.05 ve
88 eta, collagen alpha1(IV), nitrotyrosine, and mesangial matrix were all significantly increased compar