Involvement of inflammatory responses in the early development of calcific aortic valve disease: lessons from statin therapy

Lee, Seung Hyun; Choi, Jae-Hoon

doi:10.1080/19768354.2018.1528175

Cited by 16 publications

(12 citation statements)

References 99 publications

(97 reference statements)

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“…To date, researchers have attempted to elucidate the molecular pathologic mechanism of AS by investigating the roles of immune cell infiltration and resident cells, such as VICs and valvular endothelial cells (VECs), in the disease's progression. 12 , 13 , 14 , 15 These cells have been the focus of research because macrophages and T lymphocytes are major contributors to inflammation, whereas VICs function in calcification and fibrosis during disease progression. In one example, Oba and colleagues 16 found a greater distribution of CD163-positive macrophages in calcified AVs than that in noncalcified AVs and showed that the infiltrating CD163-positive macrophages were expressing high levels of bone morphogenetic protein 2.…”

Section: Discussionmentioning

confidence: 99%

Inflammatory and immune checkpoint markers are associated with the severity of aortic stenosis

et al. 2021

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Objective: Aortic stenosis (AS) is a disease characterized by narrowing of the aortic valve (AV) orifice. In relation to this disease, the purpose of this study was to elucidate the relationships among factors such as expression of programmed cell death-1 ligand (PD-L1, which is the ligand of PD-1 protein; together, they play a central role in the inhibition of T lymphocyte function), clinicopathologic characteristics, infiltrating immune cells, and disease severity.Methods: We performed immunohistochemical analysis on the surgically-resected AVs of 53 patients with AS. We used the resultant data to identify relationships among PD-L1 expression, disease severity, and the infiltration of immune cells including cluster of differentiation (CD8)-positive T lymphocytes, cluster of differentiation 163 (CD163)-positive macrophages, and forkhead box protein 3 (FOXP3)positive regulatory T lymphocytes (Tregs).Results: PD-L1 expression in resected AVs was significantly associated with being nonsmoker, valve calcification, and the infiltration of CD8-positive T cells and CD163-positive macrophages. Disease severity and valve calcification were significantly associated with low infiltration of FOXP3-positive Tregs and high infiltration of CD8-positive T cells and CD163-positive macrophages. Moreover, calcified AVs with high PD-L1 expression showed active inflammation without FOXP3-positive Tregs but with high levels of CD8-positive T lymphocytes and CD163-positive macrophages.Conclusions: Immune cell infiltration in the AVs and expression of the immune checkpoint protein PD-L1 were associated with the calcification of AS and disease severity. (JTCVS Open 2021;5:1-12)High PD-L1 and active inflammation were associated with calcified AS.

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Section: Discussionmentioning

confidence: 99%

Inflammatory and immune checkpoint markers are associated with the severity of aortic stenosis

et al. 2021

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“…IL-1b is another intriguing cytokine involved in the valve calcification process. Its levels are indeed increased in the stenotic aortic valve, making IL-1b subject to numerous research studies in the last decade (Isoda et al, 2010;Nadlonek et al, 2013;Lee and Choi, 2018). The IL-1b enhances the expression of matrix metalloproteinases (MMPs), a group of enzymes responsible for the degradation of extracellular matrix proteins.…”

Section: Innate Response In Cavdmentioning

confidence: 99%

Calcific Aortic Valve Disease-Natural History and Future Therapeutic Strategies

et al. 2020

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Calcific aortic valve disease (CAVD) is the most frequent heart valve disorder. It is characterized by an active remodeling process accompanied with valve mineralization, that results in a progressive aortic valve narrowing, significant restriction of the valvular area, and impairment of blood flow.The pathophysiology of CAVD is a multifaceted process, involving genetic factors, chronic inflammation, lipid deposition, and valve mineralization. Mineralization is strictly related to the inflammatory process in which both, innate, and adaptive immunity are involved. The underlying pathophysiological pathways that go from inflammation to calcification and, finally lead to severe stenosis, remain, however, incompletely understood. Histopathological studies are limited to patients with severe CAVD and no samples are available for longitudinal studies of disease progression. Therefore, alternative routes should be explored to investigate the pathogenesis and progression of CAVD.Recently, increasing evidence suggests that epigenetic markers such as non-coding RNAs are implicated in the landscape of phenotypical changes occurring in CAVD. Furthermore, the microbiome, an essential player in several diseases, including the cardiovascular ones, has recently been linked to the inflammation process occurring in CAVD. In the present review, we analyze and discuss the CAVD pathophysiology and future therapeutic strategies, focusing on the real and putative role of inflammation, calcification, and microbiome.

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“…The calcified aortic valve disease (CAVD) is a primary valve disease that negatively affects a high number of people worldwide ( Kirchhof et al, 2016 ). A variety of factors are involved in CAVD development, but it appears that inflammatory factors play a pivotal role ( Lee and Choi, 2018 ). The nuclear factor-kappaB (NF-κB) is suggested to induce inflammation ( Sinjari et al, 2019 ).…”

Section: Curcumin and Molecular Pathways And Mechanismsmentioning

confidence: 99%

Toward Regulatory Effects of Curcumin on Transforming Growth Factor-Beta Across Different Diseases: A Review

et al. 2020

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Immune response, proliferation, migration and angiogenesis are juts a few of cellular events that are regulated by transforming growth factor-β (TGF-β) in cells. A number of studies have documented that TGF-β undergoes abnormal expression in different diseases, e.g., diabetes, cancer, fibrosis, asthma, arthritis, among others. This has led to great fascination into this signaling pathway and developing agents with modulatory impact on TGF-β. Curcumin, a natural-based compound, is obtained from rhizome and roots of turmeric plant. It has a number of pharmacological activities including antioxidant, anti-inflammatory, anti-tumor, anti-diabetes and so on. Noteworthy, it has been demonstrated that curcumin affects different molecular signaling pathways such as Wnt/β-catenin, Nrf2, AMPK, mitogen-activated protein kinase and so on. In the present review, we evaluate the potential of curcumin in regulation of TGF-β signaling pathway to corelate it with therapeutic impacts of curcumin. By modulation of TGF-β (both upregulation and down-regulation), curcumin ameliorates fibrosis, neurological disorders, liver disease, diabetes and asthma. Besides, curcumin targets TGF-β signaling pathway which is capable of suppressing proliferation of tumor cells and invading cancer cells.

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Involvement of inflammatory responses in the early development of calcific aortic valve disease: lessons from statin therapy

Cited by 16 publications

References 99 publications

Inflammatory and immune checkpoint markers are associated with the severity of aortic stenosis

Inflammatory and immune checkpoint markers are associated with the severity of aortic stenosis

Calcific Aortic Valve Disease-Natural History and Future Therapeutic Strategies

Toward Regulatory Effects of Curcumin on Transforming Growth Factor-Beta Across Different Diseases: A Review

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