Blood pressure, hypertension and the risk of abdominal aortic aneurysms: a systematic review and meta-analysis of cohort studies

Kobeissi, Elsa; Hibino, Makoto; Pan, Han; Aune, Dagfinn

doi:10.1007/s10654-019-00510-9

Cited by 101 publications

(88 citation statements)

References 58 publications

(82 reference statements)

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“…According to the Society for Vascular Surgery practice guidelines on the care of patients with AAA, blood pressure is a potential risk factor for AAA, and men with AAA should strictly control their blood pressure. As shown in the study by Kobeissi et al (2019), hypertension increases the risk of developing AAA by 66% (Kobeissi et al, 2019). In addition, hypertension may accelerate the expansion rate of AAA and increase the risk of rupture.…”

Section: Discussionmentioning

confidence: 79%

Melatonin Plays a Critical Protective Role in Nicotine-Related Abdominal Aortic Aneurysm

Duan

Wang

et al. 2020

Front. Physiol.

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Smoking is a major risk factor for abdominal aortic aneurysm (AAA). Among the components of smoke, nicotine is known to exert pro-atherosclerotic, prothrombotic, and proangiogenic effects on vascular smooth muscle cells (VSMCs). The current study was designed to investigate the mechanisms through which nicotine induces vascular wall dysfunction and to examine whether melatonin protects against nicotine-related AAA. Methods: In this study, an enzyme-linked immunosorbent assay (ELISA) was used to measure melatonin and TNF-α levels, as well as total antioxidant status (TAS), in patients with AAA. We established a nicotine-related AAA model and explored the mechanisms underlying the therapeutic effects of melatonin. Tissue histopathology was used to assess vascular function, while western blotting (WB) and immunofluorescence staining were performed to detect protein expression. Results: We observed melatonin insufficiency in the serum from patients with AAA, particularly smokers. Moreover, melatonin level was positively correlated with antioxidant capacity. In the in vivo model, nicotine accelerated AAA expansion and destroyed vascular structure. Furthermore, OPN, LC3II, p62, matrix metalloproteinase-2 (MMP-2), matrix metalloproteinase-9 (MMP-9), NF-κB p65, TNF-α, phosphorylated AKT, and phosphorylated mTOR levels were increased, in vivo, following nicotine treatment, while SM22α and α-SMA levels were reduced. Additionally, melatonin attenuated the effects of nicotine on AAA and reversed changes in protein expression. Moreover, melatonin lost its protective effects following bafilomycin A1-mediated inhibition of autophagy. Conclusion: Based on our data, melatonin exerts a beneficial effect on rats with nicotine-related AAA by downregulating the AKT-mTOR signaling pathway, improving autophagy dysfunction, and restoring the VSMC phenotype.

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Section: Discussionmentioning

confidence: 79%

Melatonin Plays a Critical Protective Role in Nicotine-Related Abdominal Aortic Aneurysm

Duan

Wang

et al. 2020

Front. Physiol.

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“…For additional EJE references please see [142][143][144][145][146][147][148][149][150][151][152][153][154][155][156][157][158][159][160].…”

Section: Main Results In the Last 3 Yearsunclassified

Objectives, design and main findings until 2020 from the Rotterdam Study

et al. 2020

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The Rotterdam Study is an ongoing prospective cohort study that started in 1990 in the city of Rotterdam, The Netherlands. The study aims to unravel etiology, preclinical course, natural history and potential targets for intervention for chronic diseases in mid-life and late-life. The study focuses on cardiovascular, endocrine, hepatic, neurological, ophthalmic, psychiatric, dermatological, otolaryngological, locomotor, and respiratory diseases. As of 2008, 14,926 subjects aged 45 years or over comprise the Rotterdam Study cohort. Since 2016, the cohort is being expanded by persons aged 40 years and over. The findings of the Rotterdam Study have been presented in over 1700 research articles and reports. This article provides an update on the rationale and design of the study. It also presents a summary of the major findings from the preceding 3 years and outlines developments for the coming period.

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“…These data demonstrate that FA diet could represent a novel therapeutic strategy for aneurysm formation in Fbn1 C1039G/+ mice, which may be broadly useful to treat TAA of alternative causes as well. Besides oxidative stress, hypertension is considered a risk factor and mechanism for aortic aneurysms [ 46 ]. Uncoupling of eNOS has been shown to occur in spontaneously hypertensive rats (SHRs) [ 47 ], stroke-prone SHRs [ 48 ], Ang II induced hypertension [ 18 ] and hypertension induced with the DOCA [ 39 , 49 ].…”

Section: Discussionmentioning

confidence: 99%

Targeting feed-forward signaling of TGFβ/NOX4/DHFR/eNOS uncoupling/TGFβ axis with anti-TGFβ and folic acid attenuates formation of aortic aneurysms: Novel mechanisms and therapeutics

et al. 2021

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In the present study we aimed to identify novel mechanisms and therapeutics for thoracic aortic aneurysm (TAA) in Fbn1 C1039G/+ Marfan Syndrome (MFS) mice. The expression of mature/active TGFβ and its downstream effector NOX4 were upregulated while tetrahydrobiopterin (H 4 B) salvage enzyme dihydrofolate reductase (DHFR) was downregulated in Fbn1 C1039G/+ mice. In vivo treatment with anti-TGFβ completely attenuated NOX4 expression, restored DHFR protein abundance, reduced ROS production, recoupled eNOS and attenuated aneurysm formation. Intriguingly, oral administration with folic acid (FA) to recouple eNOS markedly alleviated expansion of aortic roots and abdominal aortas in Fbn1 C1039G/+ mice, which was attributed to substantially upregulated DHFR expression and activity in the endothelium to restore tissue and circulating levels of H 4 B. Notably, circulating H 4 B levels were accurately predictive of tissue H 4 B bioavailability, and negatively associated with expansion of aortic roots, indicating a novel biomarker role of circulating H 4 B for TAA. Furthermore, FA diet abrogated TGFβ and NOX4 expression, disrupting the feed-forward loop to inactivate TGFβ/NOX4/DHFR/eNOS uncoupling axis in vivo and in vitro, while PTIO, a NO scavenger, reversed this effect in cultured human aortic endothelial cells (HAECs). Besides, expression of the rate limiting H 4 B synthetic enzyme GTP cyclohydrolase 1 (GTPCHI), was downregulated in Fbn1 C1039G/+ mice at baseline. In cultured HAECs, RNAi inhibition of fibrillin resulted in reduced GTPCHI expression, while this response was abrogated by anti-TGFβ, indicating TGFβ-dependent downregulation of GTPCHI in response to fibrillin deficiency. Taken together, our data for the first time reveal that uncoupled eNOS plays a central role in TAA formation, while anti-TGFβ and FA diet robustly abolish aneurysm formation via inactivation of a novel TGFβ/NOX4/DHFR/eNOS uncoupling/TGFβ feed-forward pathway. Correction of fibrillin deficiency is additionally beneficial via preservation of GTPCHI function.

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Blood pressure, hypertension and the risk of abdominal aortic aneurysms: a systematic review and meta-analysis of cohort studies

Cited by 101 publications

References 58 publications

Melatonin Plays a Critical Protective Role in Nicotine-Related Abdominal Aortic Aneurysm

Melatonin Plays a Critical Protective Role in Nicotine-Related Abdominal Aortic Aneurysm

Objectives, design and main findings until 2020 from the Rotterdam Study

Targeting feed-forward signaling of TGFβ/NOX4/DHFR/eNOS uncoupling/TGFβ axis with anti-TGFβ and folic acid attenuates formation of aortic aneurysms: Novel mechanisms and therapeutics

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