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Target Concepts:
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Query: UMLS:C0162871 (
abdominal aortic aneurysm
)
8,664
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
A 59 years old male with
abdominal aortic aneurysm
ruptured into the left common iliac vein was transferred to us with symptoms resembling deep vein thrombosis of the left lower extremity, such as leg pain, swelling and dilatation of the superficial veins. At operation, a Fogarty's occlusion catheter was inserted through the right greater saphenous vein into the inferior vena cava and inflated concomitantly during aortic clamp to prevent pulmonary embolism which may be caused by the dislodged thrombi from the aneurysm, and as well as to control back-flow-bleeding from the central. The fistula (3.0 X 1.0cm) was closed from inside of the aneurysm using the inferior wall of the aneurysm. The blood from the fistula was collected by the Cell Saver and re-transfused to the patient. The abdominal aorta was replaced with a Dacron Y-shaped prosthesis. The postoperative course was uneventful.
CTR
on chest X-ray subsided from 51% to 42%, cardiac output normalized from 11l/min to 6l/min, and symptoms resembling the deep vein thrombosis disappeared.
...
PMID:[A case of abdominal aortic aneurysm ruptured into the left common iliac vein with symptoms resembling deep vein thrombosis]. 398 87
Background Hydrogen peroxide (H
2
O
2
) is a critical molecular signal in the development of
abdominal aortic aneurysm
(
AAA
) formation. Vascular peroxidase 1 ( VPO 1) catalyzes the production of hypochlorous acid ( HOC l) from H
2
O
2
and significantly enhances oxidative stress. The switch from a contractile phenotype to a synthetic one in vascular smooth muscle cells ( VSMC s) is driven by reactive oxygen species and is recognized as an early and important event in
AAA
formation. This study aims to determine if VPO 1 plays a critical role in the development of
AAA
by regulating VSMC phenotypic switch. Methods and Results VPO 1 is upregulated in human and elastase-induced mouse aneurysmal tissues compared with healthy control tissues. Additionally, KLF 4, a nuclear transcriptional factor, is upregulated in aneurysmatic tissues along with a concomitant downregulation of differentiated smooth muscle cell markers and an increase of synthetic phenotypic markers, indicating VSMC phenotypic switch in these diseased tissues. In cultured VSMC s from rat abdominal aorta, H
2
O
2
treatment significantly increases VPO 1 expression and HOC l levels as well as VSMC phenotypic switch. In support of these findings, depletion of VPO 1 significantly attenuates the effects of H
2
O
2
and HOC l treatment. Furthermore, HOC l treatment promotes VSMC phenotypic switch and ERK 1/2 phosphorylation. Pretreatment with U0126 (a specific inhibitor of ERK 1/2) significantly attenuates HOC l-induced VSMC phenotypic switch. Conclusions Our results demonstrate that VPO 1 modulates VSMC phenotypic switch through the H
2
O
2
/ VPO 1/ HOC l/ ERK 1/2 signaling pathway and plays a key role in the development of
AAA
. Our findings also implicate VPO 1 as a novel signaling node that mediates VSMC phenotypic switch and plays a key role in the development of
AAA
. Clinical Trial Registration URL : www.chictr.org.cn . Unique identifier: Chi
CTR
1800016922.
...
PMID:VPO1 Modulates Vascular Smooth Muscle Cell Phenotypic Switch by Activating Extracellular Signal-regulated Kinase 1/2 (ERK 1/2) in Abdominal Aortic Aneurysms. 3037 Nov 71
