Contribution of ADAM17 and related ADAMs in cardiovascular diseases

Kawai, Tatsuo; Elliott, Katherine J.; Scalia, Rosario; Eguchi, Satoru

doi:10.1007/s00018-021-03779-w

Cited by 35 publications

(30 citation statements)

References 343 publications

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“…Hence, it is not astonishing that alterations in the expression or function of these proteases are implicated in several pathologies, including cancer, rheumatoid arthritis, kidney fibrosis, diabetes, Alzheimer’s disease, and cardiovascular diseases ( Sandgren et al, 1990 ; Black et al, 1997 ; Satoh et al, 2000 ; Umemura et al, 2014 ; Kefaloyianni et al, 2016 ; Zhang et al, 2016 ; Kim et al, 2020 ; Shalaby et al, 2020 ; Adu-Amankwaah et al, 2021a ). Increasing evidence suggests that various ADAMs and other related metalloenzymes play crucial roles in cardiovascular pathophysiology via the modulation of inflammation, angiogenesis, metabolism, cell proliferation, and cell migration ( Adu-Amankwaah et al, 2021a ; Kawai et al, 2021 ). Among the ADAMs identified so far (22 in humans, 34 in mice), ADAM8, 9, 10, 12, 17, 19 and closely related metalloenzymes including MMP2, MMP9, and meprin β are associated with cardiovascular conditions such as hypertension, atherosclerosis, aortic aneurysms, restenosis, acute coronary syndrome, cardiomyopathies and HF ( Papazafiropoulou and Tentolouris, 2009 ; Broder and Becker-Pauly, 2013 ; Zhang et al, 2016 ; Adu-Amankwaah et al, 2021a ; Kawai et al, 2021 ).…”

Section: A Disintegrin and Metalloprotease 17 And Other Related Metalloproteinasesmentioning

confidence: 99%

“…In immune and non-immune cells, ADAM17 cleaves a number of substrates, including ligands of the epidermal growth factor receptor (EGFR), adhesion molecules, proinflammatory cytokines, and chemokines and their receptors. Some of these substrates include amphiregulin (AREG), epigen, epiregulin, neuregulin, tomoegulin-2, transforming growth factor-alpha (TGF-α), heparin-binding epidermal growth factor (HB-EGF), TNFα, tumor necrosis factor β (TNFβ), the TNF receptors 1 and 2 (TNFR 1 and 2), and interlukin-6 receptor (IL-6R), CXCR2, collagen XVII, desmoglein-2 and nectin-4 ( Black et al, 1997 ; Moss et al, 1997 ; Tellier et al, 2006 ; Reddy et al, 2009 ; Riethmueller et al, 2017 ; Kawai et al, 2021 ). According to Cabron et al ADAM17 is a key regulator of soluble TNFα surface levels in proinflammatory macrophages and dendritic cells ( Cabron et al, 2018 ).…”

Section: Introductionmentioning

confidence: 99%

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ADAM17, A Key Player of Cardiac Inflammation and Fibrosis in Heart Failure Development During Chronic Catecholamine Stress

Adu-Amankwaah

Adzika

Adekunle

et al. 2021

Front. Cell Dev. Biol.

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Heart failure development is characterized by persistent inflammation and progressive fibrosis owing to chronic catecholamine stress. In a chronic stress state, elevated catecholamines result in the overstimulation of beta-adrenergic receptors (βARs), specifically β2-AR coupling with Gαi protein. Gαi signaling increases the activation of receptor-stimulated p38 mitogen-activated-protein-kinases (p38 MAPKs) and extracellular signal-regulated kinases (ERKs). Phosphorylation by these kinases is a common way to positively regulate the catalytic activity of A Disintegrin and Metalloprotease 17 (ADAM17), a metalloprotease that has grown much attention in recent years and has emerged as a chief regulatory hub in inflammation, fibrosis, and immunity due to its vital proteolytic activity. ADAM17 cleaves and activates proinflammatory cytokines and fibrotic factors that enhance cardiac dysfunction via inflammation and fibrosis. However, there is limited information on the cardiovascular aspect of ADAM17, especially in heart failure. Hence, this concise review provides a comprehensive insight into the structure of ADAM17, how it is activated and regulated during chronic catecholamine stress in heart failure development. This review highlights the inflammatory and fibrotic roles of ADAM17’s substrates; Tumor Necrosis Factor α (TNFα), soluble interleukin-6 receptor (sIL-6R), and amphiregulin (AREG). Finally, how ADAM17-induced chronic inflammation and progressive fibrosis aggravate cardiac dysfunction is discussed.

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Section: A Disintegrin and Metalloprotease 17 And Other Related Metalloproteinasesmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

ADAM17, A Key Player of Cardiac Inflammation and Fibrosis in Heart Failure Development During Chronic Catecholamine Stress

Adu-Amankwaah

Adzika

Adekunle

et al. 2021

Front. Cell Dev. Biol.

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“…Increased shedding of ADAMs could induce various cardiovascular diseases, which are closely related to in ammation, tissue remodeling, and dysfunction. ADAMs may be promising therapeutic targets for hypertension and atherosclerosis [40].…”

Section: Analysis Of Potential Targetsmentioning

confidence: 99%

Research on the Mechanism of Wuwei Yuganzi San in the Treatment of Coronary Heart Disease Based on Network Pharmacology

Zhang

Guo

et al. 2021

Preprint

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Background: Coronary heart disease (CHD) is a chronic cardiovascular disease across the world, which poses numerous threats to mankind. Wuwei Yuganzi San (WYS) is a famous traditional Tibetan medicine prescription. It has been confirmed effective in the treatment of CHD, but its specific mechanism remains still unclear. Objective: To elucidate the main pharmacological action of WYS in treating CHD and investigate the underlying multiple mechanisms of its multi-ingredient-multi-target by network pharmacology.Methods: Firstly, active ingredients of WYS and connected targets of five herbs were retrieved by using traditional Chinese medicine systems pharmacology (TCMSP) and screening literature. Then, genome explanation databases (OMIM and GeneCards) were used to acquire targets related to CHD. The protein-protein interaction (PPI) network was built using the mutual targets filtering genes through protein interaction. Next, a network diagram could be established with the help of Cytoscape 3.8.2. And, STRING platform was used to construct a protein interaction network. Finally, GO and KEGG analyses were analyzed to further elucidate biological process enrichment.Results: After the screening, 36 active ingredients and 202 related targets in WYS in addition to 952 disease-related targets were acquired. A total of 37 key targets including AKT1, ESR1, and EGFR were screened in the PPI network. These targets were mostly concentrated on the transmembrane receptor protein tyrosine kinase signaling pathway, cellular response to growth factors stimulus, and response to growth factor. The KEGG enrichment demonstrated that the MAPK signaling pathway, P13K/AKT signaling pathway, Ras signaling pathway, and other corresponding signaling pathways were closely related to CHD.Conclusions. WYS plays a significant role in the treatment of CHD. And this study provides a novel approach to disclose the therapeutic mechanisms of WYS on CHD.

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“…Recalling that anti-inflammatory cytokines are secreted during PS-induced efferocytosis, it is possible to consider this as an effort to control the existing inflammatory pathology [54]. Therefore, exposure of PS on the outer plasma membrane is increased in chronic inflammatory disorders, including atherosclerotic diseases and diseases associated with coagulation disorders [53] [55], which may potentiate the activity of ADAM-17.…”

Section: Risk Factors For Covid-19 and Defective Efferocytosismentioning

confidence: 99%

Defective efferocytosis as a predictor of COVID-19 mortality

Erol¹

2021

Preprint

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COVID-19 is a generally benign coronavirus disease that can spread rapidly, except for those with a group of risk factors. Since the pathogenesis responsible for the severity of the disease has not been clearly revealed, effective treatment alternatives has not been developed. The hallmark of the SARS-CoV-2-infected cells is apoptosis. Apoptotic cells are cleared through a sterile process defined as efferocytosis by professional and nonprofessional phagocytic cells. The disease would be rapidly brought under control in the organism that can achieve effective efferocytosis, which is also a kind of innate immune response. In the risk group, the efferocytic process is defective. By the addition of the apoptotic cell load associated with SARS-COV-2 infection, failure to achieve efferocytosis of dying cells can initiate secondary necrosis that is a highly destructive process. Uncontrolled inflammation and coagulation abnormalities caused by secondary necrosis reason in various organ failures, lung in particular, which are responsible for the poor prognosis. Following the short and simplified information, this opinion paper aims to present possible treatment options that can control the severity of COVID-19 by detailing the mechanisms that can cause defective efferocytosis.

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Contribution of ADAM17 and related ADAMs in cardiovascular diseases

Cited by 35 publications

References 343 publications

ADAM17, A Key Player of Cardiac Inflammation and Fibrosis in Heart Failure Development During Chronic Catecholamine Stress

ADAM17, A Key Player of Cardiac Inflammation and Fibrosis in Heart Failure Development During Chronic Catecholamine Stress

Research on the Mechanism of Wuwei Yuganzi San in the Treatment of Coronary Heart Disease Based on Network Pharmacology

Defective efferocytosis as a predictor of COVID-19 mortality

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