Differential mRNA expression of inflammasome genes NLRP1 and NLRP3 in abdominal aneurysmal and occlusive aortic disease

Gonzalez-Hidalgo, Carmen; Haro, Joaquín De; Bleda, Silvia; Cañibano, Cristina; Michel, Ignacio; Aciń, Francisco

doi:10.1177/1753944718750338

Cited by 5 publications

(7 citation statements)

References 28 publications

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“…Single-nucleotide polymorphisms in NLRP1 are associated with an increased risk of developing type-1 diabetes and systemic lupus erythematosus (SLE) in Brazilian population cohorts ( 113 ). Patients with aortic occlusive disease (AOD) have exhibited higher mRNA expression of NLRP1 than healthy individuals ( 153 ).…”

Section: Inflammasomes In Chronic Inflammatory Disordersmentioning

confidence: 99%

Cannabinoids as Key Regulators of Inflammasome Signaling: A Current Perspective

Suryavanshi

Kovalchuk

2021

Front. Immunol.

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Inflammasomes are cytoplasmic inflammatory signaling protein complexes that detect microbial materials, sterile inflammatory insults, and certain host-derived elements. Inflammasomes, once activated, promote caspase-1–mediated maturation and secretion of pro-inflammatory cytokines, interleukin (IL)-1β and IL-18, leading to pyroptosis. Current advances in inflammasome research support their involvement in the development of chronic inflammatory disorders in contrast to their role in regulating innate immunity. Cannabis (marijuana) is a natural product obtained from the Cannabis sativa plant, and pharmacologically active ingredients of the plant are referred to as cannabinoids. Cannabinoids and cannabis extracts have recently emerged as promising novel drugs for chronic medical conditions. Growing evidence indicates the potent anti-inflammatory potential of cannabinoids, especially Δ9-tetrahydrocannabinol (Δ9-THC), cannabidiol (CBD), and synthetic cannabinoids; however, the mechanisms remain unclear. Several attempts have been made to decipher the role of cannabinoids in modulating inflammasome signaling in the etiology of chronic inflammatory diseases. In this review, we discuss recently published evidence on the effect of cannabinoids on inflammasome signaling. We also discuss the contribution of various cannabinoids in human diseases concerning inflammasome regulation. Lastly, in the milieu of coronavirus disease-2019 (COVID-19) pandemic, we confer available evidence linking inflammasome activation to the pathophysiology of COVID-19 suggesting overall, the importance of cannabinoids as possible drugs to target inflammasome activation in or to support the treatment of a variety of human disorders including COVID-19.

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Section: Inflammasomes In Chronic Inflammatory Disordersmentioning

confidence: 99%

Cannabinoids as Key Regulators of Inflammasome Signaling: A Current Perspective

Suryavanshi

Kovalchuk

2021

Front. Immunol.

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“…2,23 Therefore, blocking or inhibiting the activation of NLRP3 may become a novel therapeutic target for ischemic cerebrovascular disease. 23 This data, Beclin1/NLRP3 signal pathway is a critical downstream effector of DAPK1 by ATP production. Oikonomou et al 24 showed that noncanonical fungal autophagy inhibits inflammation in response to IFN-γ via DAPK1/NLRP3 activation.…”

Section: Discussionmentioning

confidence: 99%

DAPK1 may be a potential biomarker for arterial aneurysm in clinical treatment and activated inflammation levels in arterial aneurysm through NLRP3 inflammasome by Beclin1

Cheng

et al. 2021

Hum Exp Toxicol

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Background Death-associated protein kinase (DAPK1) is one of the positive regulators of apoptosis, and it is widely involved in apoptosis induced by multiple pathways. We examined that the function of DAPK1 in Clinical treatment of arterial aneurysm and its underlying mechanisms. Arterial aneurysm is a common cerebrovascular disease with high disability and fatality rate. Objectives Male C57BL/6 mice or DAPK1−/− mice were injected with 50 mg/kg pentobarbital sodium and then were injected with angiotensin II (AngII) infusion for vivo model. hASMCs (Human artery smooth muscle cell) were treated with murine recombinant IL-6 (20 ng ml−1; Cell Signaling) for vitro model. Results DAPK1 gene, mRNA expression, and protein expression were induced in mice of arterial aneurysm. DAPK1 mRNA expression was increased and Area Under Curve was 0.9075 in patients with arterial aneurysm. Knockout of DAPK1 decreased inflammation and vascular injury in mice model of arterial aneurysm. Beclin1/NLRP3 (NACHT, LRR, and PYD domains-containing protein 3) signal pathway is a critical downstream effector of DAPK1 by TAP production. The regulation of Beclin1 participated in the effects of DAPK1 on inflammation of arterial aneurysm by ATP-dependent NLRP3 inflammasome. The regulation of NLRP3 participated in the effects of DAPK1 on inflammation of arterial aneurysm. Conclusion Collectively, our data indicated that DAPK1 may be a potential biomarker for arterial aneurysm in clinical treatment and activated inflammation levels in arterial aneurysm through NLRP3 inflammasome by Beclin1. DAPK1 might be a key pathogenic event underlying excess inflammation of arterial aneurysm.

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“…33 With the progress of research, increasing evidence shows that inflammation plays an important role in the occurrence and development of TAAs. 6,22 As an indicator of systemic inflammation, LMR is also a routine and economical detection index for patients, which can provide a reference for the clinical treatment of patients to a certain extent. There are a few limitations to this study.…”

Section: Discussionmentioning

confidence: 99%

“…4 Recent studies have shown that multiple inflammation-related factors are closely associated with the pathogenesis of TAAs. 5,6 The main pathological manifestations of TAA are continuous dilation of the artery caused by the invasion of inflammatory cells, destruction of the middle elastic protein matrix, inflammatory cell infiltration in the aortic wall, thrombosis in the lumen, and elevated C-reactive protein (CRP) levels. [7][8][9] In the progression of TAA, the expression of inflammatory cells within the aneurysmal wall increased and the serum proinflammatory cytokines were elevated.…”

Section: Introductionmentioning

confidence: 99%

Preoperative high lymphocyte-to-monocyte ratio is associated with intraoperative type I endoleak in patients with TAA with TEVAR

Xie

Zhao

et al. 2021

Vascular

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Objectives Various inflammatory factors are closely associated with the incidence of thoracic aortic aneurysms (TAAs). Furthermore, the severity of inflammation is closely related to the absolute value and proportion of each leukocyte subgroup. Only few reports have analyzed the importance of lymphocyte–monocyte ratio (LMR) as a potential inflammatory marker in vascular diseases. Therefore, we aimed to investigate the effect of peripheral blood LMR on thoracic endovascular aortic repair (TEVAR) in patients with TAA. Methods A retrospective study of the clinical data collected in our hospital between January 2016 and January 2021 was performed on 162 patients with TAA treated with TEVAR, based on the inclusion and exclusion criteria for patient selection. Based on whether the patient had the clinical symptoms at admission and the occurrence of type I endoleaks during operation, patients were divided into two groups, respectively: an intraoperative type I endoleak group ( n = 34) and a group without intraoperative type I endoleak ( n = 128), and a group with clinical symptoms ( n = 31) and a group without clinical symptoms ( n = 131). The clinical data of these two groups were compared, the free from second intervention rates related to endoleak and the preoperatively LMR of the two groups was calculated. LMR was calculated preoperatively. Receiver-operating characteristic curve analysis was used to determine the cut-off for preoperative LMR values. Based on the cut-off point, patients were divided into a high LMR group ( n = 34) and a low LMR group ( n = 128). The clinical data of the two groups were compared, and further stratified analysis was performed. Results A total of 162 patients were included in the analysis. All patients were successfully implanted with a thoracic aorta stent graft. The preoperative LMR level and postoperative endoleak-related secondary intervention rate were higher in the type I endoleak group than those in the group without intraoperative type I endoleaks. The preoperative C-reactive protein (CRP) level of patients with TAA with clinical symptoms was higher than that of asymptomatic patients. There was a negative correlation between preoperative CRP and LMR levels. In addition, in symptomatic or asymptomatic patients, the LMR level was associated with the occurrence of intraoperative type I endoleaks. After excluding the influence of type of endografts, our results showed that the clinical symptoms did not affect the occurrence of the intraoperative type I endoleak, and patients with intraoperative type I endoleak had a higher rate of postoperative secondary intervention. Conclusion Patients with TAA with type I endoleaks during TEVAR had an increased rate of secondary intervention related to endoleaks. Patients with TAA with high LMR levels before TEVAR were more likely to have endoleaks during operation.

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Differential mRNA expression of inflammasome genes NLRP1 and NLRP3 in abdominal aneurysmal and occlusive aortic disease

Cited by 5 publications

References 28 publications

Cannabinoids as Key Regulators of Inflammasome Signaling: A Current Perspective

Cannabinoids as Key Regulators of Inflammasome Signaling: A Current Perspective

DAPK1 may be a potential biomarker for arterial aneurysm in clinical treatment and activated inflammation levels in arterial aneurysm through NLRP3 inflammasome by Beclin1

Preoperative high lymphocyte-to-monocyte ratio is associated with intraoperative type I endoleak in patients with TAA with TEVAR

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