The expression of inhibitor of nuclear factor kappa-B kinase epsilon (IKKe) in human aortic aneurysm

Zhang, L; Wang, L; Chen, W; Xu, Yueyue; Iskandar, Reinard; Wang, Y; X, Chen

doi:10.5603/fm.a2017.0016

Cited by 2 publications

(2 citation statements)

References 16 publications

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“…Therefore, it was inferred that IKKε plays an important role in AAA development. A previous study revealed that IKKε expression is significantly increased in patients with AAA ( 10 ). The results of a another study indicated that the lack of IKKε reduced AAA formation by reducing apoptosis and inflammation in the abdominal aorta of mice ( 11 ).…”

Section: Introductionmentioning

confidence: 97%

IKKε knockout alleviates angiotensin II‑induced apoptosis and excessive autophagy in vascular smooth muscle cells by regulating the ERK1/2 pathway

Chen

Yao

et al. 2021

Exp Ther Med

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Inhibitor of nuclear factor-κB kinase subunit ε (IKKε) is an important signal regulator in the formation of abdominal aortic aneurysm (AAA). However, the underlying mechanism remains to be elucidated. Therefore, the present study aimed to investigate the mechanism underlying IKKε function in AAA formation by studying apoptosis and autophagy in angiotensin II (Ang II)-induced vascular smooth muscle cells (VSMCs). AngⅡ was used to stimulate VSMCs for 24 h to simulate the process of AAA formation. VSMCs were transfected with IKKε small interfering RNA to investigate the effect of IKKε on AAA formation, cell apoptosis and autophagy. IKKε deficiency led to reduced mitochondrial damage and apoptosis in VSMCs in the early stage of apoptosis in vitro, as demonstrated using a JC-1 probe. IKKε deficiency also reduced autophagy and decreased the formation of autophagic vacuoles in VSMCs, demonstrated using transmission electron microscopy. The decrease in apoptosis caused by IKKε knockdown was reversed when the autophagic flow was blocked using bafilomycin A1. Western blot analysis further revealed that IKKε deficiency negatively regulated the ERK1/2 signaling pathway to reduce autophagy. Collectively, the results of the present study revealed that IKKε played a key role in apoptosis by inducing excessive autophagy, thereby potentially contributing to AAA formation. These findings further revealed the mechanism underlying IKKε function in the formation of AAA.

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Section: Introductionmentioning

confidence: 97%

IKKε knockout alleviates angiotensin II‑induced apoptosis and excessive autophagy in vascular smooth muscle cells by regulating the ERK1/2 pathway

Chen

Yao

et al. 2021

Exp Ther Med

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“…TAA, in addition to conventional risk factors, exhibits a strong heritable pattern [3]. Existing evidences show that AAA and TAA share similarities in pathological states and histological phenotypes, including inflammatory reaction and extracellular matrix (ECM) degeneration in aortic wall [4,5].…”

Section: Introductionmentioning

confidence: 99%

TLR4 and MMP2 polymorphisms and their associations with cardiovascular risk factors in susceptibility to aortic aneurysmal diseases

Li¹,

Sun²,

Jiang

et al. 2019

Bioscience Reports

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Background: Toll-like receptor 4 (TLR4) and matrix metalloproteinase 2 (MMP2) play important roles in aortic pathophysiology. We aimed to evaluate the contribution of TLR4 and MMP2 polymorphisms individually and complex interactions between gene and risk factors in susceptibility to aortic aneurysm (AA) and its subtypes. Methods: KASP method was adopted to detect TLR4rs11536889, rs1927914 and MMP2rs2285053 polymorphisms in 498 controls and 472 AA patients, including 212 abdominal AA (AAA) and 216 thoracic AA (TAA). Results: In the overall analysis, MMP2rs2285053 TC genotype was correlated with TAA risk (P = 0.047, OR = 1.487). Stratified analysis revealed an increased AA risk in males with TLR4rs1927914 TC genotype, while MMP2rs2285053 TC conferred an elevated AA risk in the subjects ≤60 years, and its TC genotype and dominant model were associated with TAA in the subjects ≤60 year. The interaction between TLR4rs1927914 and MMP2rs2285053 was associated with AAA risk (Pinteraction = 0.028, OR = 2.913). Furthermore, significant interaction between TLR4rs11536889 and dyslipidemia was observed for TAA risk, while TLR4rs1927914 could interact with hypertension and diabetes to increase the risk of AA or its subtypes. Two-way interaction effect of TLR4rs1927914 and MMP2rs2285053 was enhanced by diabetes or dyslipidemia. Conclusion: TLR4 and MMP2 polymorphisms and their complex interactions with cardiovascular risk factors contributed to aortic aneurysmal diseases.

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The expression of inhibitor of nuclear factor kappa-B kinase epsilon (IKKe) in human aortic aneurysm

Abstract: (Folia Morphol 2017; 76, 3: 372-378)

Cited by 2 publications

References 16 publications

IKKε knockout alleviates angiotensin II‑induced apoptosis and excessive autophagy in vascular smooth muscle cells by regulating the ERK1/2 pathway

IKKε knockout alleviates angiotensin II‑induced apoptosis and excessive autophagy in vascular smooth muscle cells by regulating the ERK1/2 pathway

TLR4 and MMP2 polymorphisms and their associations with cardiovascular risk factors in susceptibility to aortic aneurysmal diseases

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