Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0162871 (abdominal aortic aneurysm)
 8,664 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The indications for open abdominal aortic aneurysm (AAA) repair have changed with the development of endovascular techniques. The purpose of this study is to clarify the indications and outcomes for open repair since endovascular aneurysm repair (EVAR) and to compare contemporary AAA repair with the pre-EVAR era. Patients undergoing open AAA repair were identified; the demographics, outcomes, and indications for open repair were reviewed. Outcomes were compared based on indication for open repair in the EVAR era and between the pre-EVAR and EVAR eras. Open indications in the EVAR era included: age younger than 65 years with minimal comorbidities (AGE, n = 24 [9.8%]), unfavorable anatomy (ANAT, n = 146 [59.3%]), aortoiliac occlusive disease (AIOD, n = 38 [15.4%]), and miscellaneous (OTHER, n = 38 [15.4%]). Mortality (30-day and 5-year) was affected by indication: AGE = 0 and 0 per cent, ANAT = 4.1 and 49.7 per cent, AIOD = 13.5 and 32.3 per cent, and OTHER = 5.3 and 41.8 per cent. Age, sex, race, coronary artery disease, and peripheral artery disease were similar between the pre-EVAR and EVAR eras. EVAR-era patients had more diabetes mellitus, hypertension, and hyperlipidemia and longer operative time. Mortality was not different, but complication rates were lower in the pre-EVAR era (23.7 vs 43.5%, P = 0.025). Patients undergoing open AAA repair in the EVAR era have more comorbidities, longer operative times, and more complications. Outcomes for EVAR-era patients are affected by the indication for open repair. A preference for open repair in younger patients with minimal comorbidities is justified.
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PMID:Changing indications and outcomes for open abdominal aortic aneurysm repair since the advent of endovascular repair. 1972 88

Abdominal aortic aneurysm (AAA) is a fatal disease, and exposure to 3,4-benzopyrene (Bap) is closely related to the development of AAA. We have found that Bap could impair the biological function of endothelial progenitor cells (EPCs), which are associated with the occurrence of AAA. We have also demonstrated that macrophage activation plays a key role in Bap-induced AAA, but the mechanism is unknown. Here, we used a mouse lncRNA array to investigate the expression signatures of lncRNAs and mRNAs in Bap-activated macrophage. A total of 457 lncRNAs and 219 mRNAs were found to be differentially expressed. The function of differential mRNAs was determined by pathway and Gene Ontology analysis. Eight pathways associated with inflammation were upregulated, and seven pathways including cell apoptosis were downregulated. It was worth noting that AGE-RAGE pathway, which was involved in Bap-induced EPC dysfunction, was significantly upregulated in Bap-activated macrophage and may contribute to AAA formation. Thus, lncRNAs may exert a key role in activated macrophages and intervene the core lncRNAs and may inhibit the occurrence of a series of cascade reactions in the macrophages, which may provide potential targets for AAA caused by smoking.
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PMID:Microarray Analysis Reveals a Potential Role of lncRNA Expression in 3,4-Benzopyrene/Angiotensin II-Activated Macrophage in Abdominal Aortic Aneurysm. 2918 Oct 36

Aortic aneurysms are mostly asymptomatic but have high rates of mortality when there is rupture or dissection. Matrix metalloproteinases is involved in the evolution of aortic aneurysms. Advanced glycation end products and its cell receptor RAGE (receptor for AGE) and sRAGE (soluble receptor of AGE) have been suggested to be involved in the pathogenesis of numerous diseases. This review addresses the role of AGE, RAGE and AGE-RAGE stress (AGE/sRAGE) in the pathogenesis of abdominal aortic aneurysm and thoracic aortic aneurysm in humans. AGERAGE interaction not only increases the generation of reactive oxygen species and inflammatory cytokines, but also activates NF-kB. There are increases in the levels of AGE in aortic tissue, skin and serum in patients with thoracic aortic aneurysm and abdominal aortic aneurysm. Levels of RAGE in tissue are elevated in abdominal aortic aneurysm. AGE-RAGE stress is elevated in patients with thoracic aortic aneurysm. The serum levels of cytokines and Matrix metalloproteinases are elevated in patients with thoracic aortic aneurysm and abdominal aortic aneurysm. The levels of AGE and AGE-RAGE stress correlate positively with cytokines and Matrix metalloproteinases, but the serum levels of sRAGE correlate negatively with cytokines and Matrix metalloproteinases. Cytokines levels are positively correlated with the levels of Matrix metalloproteinases in patients with thoracic aortic aneurysm. In conclusion, elevated levels of AGE, RAGE and AGE-RAGE stress, and reduced levels of sRAGE increase the levels of cytokines that in turn increase the production of Matrix metalloproteinases resulting in formation of aortic aneurysms. The data suggest that AGE-RAGE stress is involved in the pathogenesis of aortic aneurysms. Treatment options have also been discussed.
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PMID:AGE-RAGE stress play a role in aortic aneurysm: A comprehensive review and novel potential therapeutic target. 3191 11