Haem-Enzymes Predictive of Coronary Artery Disease Are Present in Thoracic and Abdominal Aortic Aneurysm

Sherrah, Andrew G.; Wilson, Michael K.; Thomas, Shane; Chan, Enoch; Yeung, Amanda; Robertson, E.; Jeremy, Richmond W.; Hambly, Brett D.; Qasabian, Raffi; Vallely, Michael P.; Bannon, Paul G.

doi:10.1016/j.hlc.2017.03.147

Cited by 2 publications

(3 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Elevated levels of the pro-inflammatory enzyme myeloperoxidase (MPO) are widely implicated in the pathogenesis of AAA [72][73][74], intracranial aneurysms [75][76][77], in other cardiovascular diseases [78], and in inflammation across multiple body systems [79]. MPO, a haem peroxidase, is produced predominantly by neutrophils [80], and its expression in vascular inflammation is localised to the endothelium and sub-endothelial space [78].…”

Section: Excess Ros Generationmentioning

confidence: 99%

“…Increased MPO has been observed in aortic wall specimens from a mixed cohort of TAA patients [ 72 ]. Additionally, a MFS mouse model showed increased MPO expression in the aneurysmal aorta, along with increased MMP-2 and -9 expression, increased ECM fragmentation and apoptosis, increased 3-nitrotyrosine levels and increased ROS staining compared to wildtype [ 87 ].…”

Section: Sources Of Ros Imbalancementioning

confidence: 99%

See 1 more Smart Citation

Oxidative stress in genetically triggered thoracic aortic aneurysm: role in pathogenesis and therapeutic opportunities

et al. 2021

View full text Add to dashboard Cite

Background: The primary objective of this review was to explore the contribution of oxidative stress to the pathogenesis of genetically-triggered thoracic aortic aneurysm (TAA). Genetically-triggered TAAs manifest substantial variability in onset, progression, and risk of aortic dissection, posing a significant clinical management challenge. There is a need for non-invasive biomarkers that predict the natural course of TAA and therapeutics that prevent aneurysm progression. Methods: An online systematic search was conducted within PubMed, MEDLINE, Scopus and ScienceDirect databases using keywords including: oxidative stress, ROS, nitrosative stress, genetically triggered thoracic aortic aneurysm, aortic dilatation, aortic dissection, Marfan syndrome, Bicuspid Aortic Valve, familial TAAD, Loeys Dietz syndrome, and Ehlers Danlos syndrome. Results: There is extensive evidence of oxidative stress and ROS imbalance in genetically triggered TAA. Sources of ROS imbalance are variable but include dysregulation of redox mediators leading to either insufficient ROS removal or increased ROS production. Therapeutic exploitation of redox mediators is being explored in other cardiovascular conditions, with potential application to TAA warranting further investigation. Conclusion: Oxidative stress occurs in genetically triggered TAA, but the precise contribution of ROS to pathogenesis remains incompletely understood. Further research is required to define causative pathological relationships in order to develop therapeutic options.

show abstract

Section: Excess Ros Generationmentioning

confidence: 99%

Section: Sources Of Ros Imbalancementioning

confidence: 99%

Oxidative stress in genetically triggered thoracic aortic aneurysm: role in pathogenesis and therapeutic opportunities

et al. 2021

View full text Add to dashboard Cite

show abstract

“…Increased MPO has been observed in the aortic wall of a mixed cohort of patients requiring surgical resection for TAA, with MPO expressed within the intimal and medial layers [ 119 ]. Additionally, in a small study of BAV patients, plasma MPO has been specifically associated with valvular dysfunction, but no effect was seen on TAA development or progression in this underpowered study [ 120 ].…”

Section: Mpo-associated Oxidative Stress and Links To Taa Pathogenmentioning

confidence: 99%

The Role of Inflammation and Myeloperoxidase-Related Oxidative Stress in the Pathogenesis of Genetically Triggered Thoracic Aortic Aneurysms

Malecki

Hambly

Jeremy

et al. 2020

IJMS

View full text Add to dashboard Cite

Genetically triggered thoracic aortic aneurysms (TAAs) are usually considered to exhibit minimal levels of inflammation. However, emerging data demonstrate that specific features of an inflammatory response can be observed in TAA, and that the extent of the inflammatory response can be correlated with the severity, in both mouse models and in human studies. Myeloperoxidase (MPO) is a key mediator of the inflammatory response, via production of specific oxidative species, e.g., the hypohalous acids. Specific tissue modifications, mediated by hypohalous acids, have been documented in multiple cardiovascular pathologies, including atherosclerosis associated with coronary artery disease, abdominal aortic, and cerebral aneurysms. Similarly, data are now emerging that show the capacity of MPO-derived oxidative species to regulate mechanisms important in TAA pathogenesis, including alterations in extracellular matrix homeostasis, activation of matrix metalloproteinases, induction of endothelial dysfunction and vascular smooth muscle cell phenotypic switching, and activation of ERK1/2 signaling. The weight of evidence supports a role for inflammation in exacerbating the severity of TAA progression, expanding our understanding of the pathogenesis of TAA, identifying potential biomarkers for early detection of TAA, monitoring severity and progression, and for defining potential novel therapeutic targets.

show abstract

Haem-Enzymes Predictive of Coronary Artery Disease Are Present in Thoracic and Abdominal Aortic Aneurysm

Cited by 2 publications

References 0 publications

Oxidative stress in genetically triggered thoracic aortic aneurysm: role in pathogenesis and therapeutic opportunities

Oxidative stress in genetically triggered thoracic aortic aneurysm: role in pathogenesis and therapeutic opportunities

The Role of Inflammation and Myeloperoxidase-Related Oxidative Stress in the Pathogenesis of Genetically Triggered Thoracic Aortic Aneurysms

Contact Info

Product

Resources

About