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1 d fractional shortening and interstitial and perivascular fibrosis.
2 PAI-1 promotes the development of perivascular fibrosis.
3 se (NOS) is known to induce hypertension and perivascular fibrosis.
4 icular hypertrophy, multifocal fibrosis, and perivascular fibrosis.
5 eposition, along with a similar reduction in perivascular fibrosis.
6 rdiomyocyte hypertrophy and interstitial and perivascular fibrosis.
7 , resulted in approximately 50% reduction of perivascular fibrosis after transverse aortic constricti
9 as shown by reduced LV volumes, wall stress, perivascular fibrosis, and cardiac lipid accumulation.
10 zone did not affect LV remodeling, increased perivascular fibrosis, and promoted further cardiac lipi
11 d significantly more intimal hyperplasia and perivascular fibrosis compared to wild-type mice followi
12 n contrast, coronary arterial thickening and perivascular fibrosis, determined by the media/lumen-are
13 etent mice, persistent PH is associated with perivascular fibrosis; iii) elevated levels of the fibro
15 nges in systolic blood pressure and coronary perivascular fibrosis in PAI-1-deficient (PAI-1(-/-)) an
16 l remodeling, such as medial hypertrophy and perivascular fibrosis in response to pressure overload,
18 nase kinase 6-p38 developed interstitial and perivascular fibrosis in the heart, lung, and kidney as
21 a1 hl/u]-RT1.Aa molecules revealed only mild perivascular fibrosis, minimal intimal thickening, and p
22 nlarged, fat-laden hepatocytes together with perivascular fibrosis narrowed sinusoidal lumens, making
23 ly accompanied by intensive interstitial and perivascular fibrosis, which may contribute to arrhythmo
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