Relationship between inflammatory-related cytokines with aortic dissection

Song, Jingjin; Peng, Hua; Lai, Min; Hj, Kang; Chen, X; Cheng, Ye; Su, Xin

doi:10.1016/j.intimp.2023.110618

Cited by 5 publications

(2 citation statements)

References 87 publications

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“…The deposition of fibrinogen, a target of native IgG, was observed to occur prior to the onset of aortic dissection [ 33 ]. This abnormal infiltration of pro-inflammatory cells into the aortic wall subsequently triggered apoptosis of vascular smooth muscle cells (VSMCs) and induced the abnormal expression of pro-inflammatory cytokines such as tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interferon (IF) [ 34 ]. The apoptotic process of vascular smooth muscle cells (VSMCs) within the medial layer of the vasculature, as well as the dysfunction of VSMCs, are significant factors in the pathogenesis and progression of aortic dissection [ 29 , 35 ].…”

Section: Discussionmentioning

confidence: 99%

Diabetes and aortic dissection: unraveling the role of 3-hydroxybutyrate through mendelian randomization

Qiu,

Liu,

Jiang

et al. 2024

Cardiovasc Diabetol

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Background In observational and experimental studies, diabetes has been reported as a protective factor for aortic dissection. 3-Hydroxybutyrate, a key constituent of ketone bodies, has been found to favor improvements in cardiovascular disease. However, whether the protective effect of diabetes on aortic dissection is mediated by 3-hydroxybutyrate is unclear. We aimed to investigate the causal effects of diabetes on the risk of aortic dissection and the mediating role of 3-hydroxybutyrate in them through two-step Mendelian randomization. Materials and methods We performed a two-step Mendelian randomization to investigate the causal connections between diabetes, 3-hydroxybutyrate, and aortic dissection and calculate the mediating effect of 3-hydroxybutyrate. Publicly accessible data for Type 1 diabetes, Type 2 diabetes, dissection of aorta and 3-hydroxybutyrate were obtained from genome-wide association studies. The association between Type 1 diabetes and dissection of aorta, the association between Type 2 diabetes and dissection of aorta, and mediation effect of 3-hydroxybutyrate were carried out separately. Results The IVW method showed that Type 1 diabetes was negatively associated with the risk of aortic dissection (OR 0.912, 95% CI 0.836–0.995), The weighted median, simple mode and weighted mode method showed consistent results. The mediated proportion of 3-hydroxybutyrate on the relationship between Type 1 diabetes and dissection of aorta was 24.80% (95% CI 5.12–44.47%). The IVW method showed that Type 2 diabetes was negatively associated with the risk of aortic dissection (OR 0.763, 95% CI 0.607–0.960), The weighted median, simple mode and weighted mode method showed consistent results. 3-Hydroxybutyrate does not have causal mediation effect on the relationship between Type 2 diabetes and dissection of aorta. Conclusion Mendelian randomization study revealed diabetes as a protective factor for dissection of aorta. The protective effect of type 1 diabetes on aortic dissection was partially mediated by 3-hydroxybutyrate, but type 2 diabetes was not 3-hydroxybutyrate mediated. Graphical abstract

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Section: Discussionmentioning

confidence: 99%

Diabetes and aortic dissection: unraveling the role of 3-hydroxybutyrate through mendelian randomization

Qiu,

Liu,

Jiang

et al. 2024

Cardiovasc Diabetol

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“…Upon caspase-1 activation, precursor forms of IL-1β and IL-18 are processed to their mature active state 56 . Pro-inflammatory cytokines, such as TNF-α, IL-1β, IL-8, and IFN-γ, play important roles in the formation and development of AD 57 . In this investigation, LILRB4 knockdown suppressed the protein expression of NLRP3, GSDMD-N, and cleaved-caspase-1 and reduced the expression levels of TNF-α, IL-1β, IL-8 and IFN-γ.…”

Section: Discussionmentioning

confidence: 99%

LILRB4 knockdown inhibits aortic dissection development by regulating pyroptosis and the JAK2/STAT3 signaling pathway

Xiong,

Ling,

Yan

et al. 2024

Sci Rep

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Aortic dissection (AD) is a life-threatening condition with a high mortality rate and without effective pharmacological therapies. Our previous study illustrated that leukocyte immunoglobulin-like receptor B4 (LILRB4) knockdown promoted the contractile phenotypic switch and apoptosis of AD cells. This study aimed to further investigate the role of LILRB4 in animal models of AD and elucidate its underlying molecular mechanisms. Animal models of AD were established using 0.1% beta-aminopropionitrile and angiotensin II and an in vitro model was developed using platelet-derived growth factor BB (PDGF-BB). The effects of LILRB4 knockdown on histopathological changes, pyroptosis, phenotype transition, extracellular matrix (ECM), and Janus kinase 2 (JAK2)/signal transducers and activators of transcription 3 (STAT3) pathways were assessed using a series of in vivo and in vitro assays. The effects of the JAK2 inhibitor AG490 on AD cell function, phenotypic transition, and ECM were explored. LILRB4 was highly expressed in AD and its knockdown increased survival rate, reduced AD incidence, and alleviated histopathological changes in the AD mouse model. Furthermore, LILRB4 knockdown promoted contractile phenotype switch, stabilized the ECM, and inhibited pyroptosis. Mechanistically, LILRB4 knockdown inhibited the JAK2/STAT3 signaling pathway. JAK2 inhibitor AG490 inhibited cell viability and migration, enhanced apoptosis, induced G0/G1 cell cycle arrest, and suppressed S-phase progression in PDGF-BB-stimulated human aortic smooth muscle cells. LILRB4 knockdown suppresses AD development by inhibiting pyroptosis and the JAK2/STAT3 signaling pathway.

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EDIL3/Del-1 prevents aortic dissection through enhancing internalization and degradation of apoptotic vascular smooth muscle cells

Yin,

Zhang,

Zhao

et al. 2024

Autophagy

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Relationship between inflammatory-related cytokines with aortic dissection

Cited by 5 publications

References 87 publications

Diabetes and aortic dissection: unraveling the role of 3-hydroxybutyrate through mendelian randomization

Diabetes and aortic dissection: unraveling the role of 3-hydroxybutyrate through mendelian randomization

LILRB4 knockdown inhibits aortic dissection development by regulating pyroptosis and the JAK2/STAT3 signaling pathway

EDIL3/Del-1 prevents aortic dissection through enhancing internalization and degradation of apoptotic vascular smooth muscle cells

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