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1 eposition, along with a similar reduction in perivascular fibrosis.
2 rdiomyocyte hypertrophy and interstitial and perivascular fibrosis.
3 d fractional shortening and interstitial and perivascular fibrosis.
4 PAI-1 promotes the development of perivascular fibrosis.
5 se (NOS) is known to induce hypertension and perivascular fibrosis.
6 icular hypertrophy, multifocal fibrosis, and perivascular fibrosis.
7 injury, renal macrophage accrual, and renal perivascular fibrosis.
8 y density is accompanied by interstitial and perivascular fibrosis.
9 es per mm(2) accompanied by interstitial and perivascular fibrosis.
11 , resulted in approximately 50% reduction of perivascular fibrosis after transverse aortic constricti
12 nic mice develop interstitial myocardial and perivascular fibrosis and left ventricular hypertrophy a
14 as shown by reduced LV volumes, wall stress, perivascular fibrosis, and cardiac lipid accumulation.
15 zone did not affect LV remodeling, increased perivascular fibrosis, and promoted further cardiac lipi
16 rgest decrease in the medial wall thickness, perivascular fibrosis, and vascular cell proliferation,
17 d significantly more intimal hyperplasia and perivascular fibrosis compared to wild-type mice followi
18 ells into RAG1(-/-) mice resulted in reduced perivascular fibrosis compared with the effect of WT T c
19 n contrast, coronary arterial thickening and perivascular fibrosis, determined by the media/lumen-are
21 mmation, myocyte apoptosis, interstitial and perivascular fibrosis, endothelial-mesenchymal transitio
22 etent mice, persistent PH is associated with perivascular fibrosis; iii) elevated levels of the fibro
24 T-cell-derived miR-214 controls pathological perivascular fibrosis in hypertension mediated by T cell
25 importance of vascular stiffening linked to perivascular fibrosis in hypertension, the molecular and
26 a model revealed that cachectic mice develop perivascular fibrosis in major metabolic organs, includi
27 nges in systolic blood pressure and coronary perivascular fibrosis in PAI-1-deficient (PAI-1(-/-)) an
28 l remodeling, such as medial hypertrophy and perivascular fibrosis in response to pressure overload,
29 enhancer-1, and endothelin-1 expression and perivascular fibrosis in SS mice at 3 days after H/R str
31 nase kinase 6-p38 developed interstitial and perivascular fibrosis in the heart, lung, and kidney as
34 a1 hl/u]-RT1.Aa molecules revealed only mild perivascular fibrosis, minimal intimal thickening, and p
35 nlarged, fat-laden hepatocytes together with perivascular fibrosis narrowed sinusoidal lumens, making
36 patterns were different, with periductal and perivascular fibrosis occurring more frequently in T1D p
37 cytosis, and moderate splenomegaly with mild perivascular fibrosis of the spleen persist even in the
38 ly accompanied by intensive interstitial and perivascular fibrosis, which may contribute to arrhythmo
39 xpression of fetal genes and coronary artery perivascular fibrosis, with ischaemia indicated by enhan
40 ce, -1.3 [95% CI, -2.5 to -0.2]; P=0.016 for perivascular fibrosis), worse cardiac dysfunction (mean