We are analyzing https://link.springer.com/article/10.1007/s00018-021-03779-w.

Title:
Contribution of ADAM17 and related ADAMs in cardiovascular diseases | Cellular and Molecular Life Sciences
Description:
A disintegrin and metalloproteases (ADAMs) are key mediators of cell signaling by ectodomain shedding of various growth factors, cytokines, receptors and adhesion molecules at the cellular membrane. ADAMs regulate cell proliferation, cell growth, inflammation, and other regular cellular processes. ADAM17, the most extensively studied ADAM family member, is also known as tumor necrosis factor (TNF)-α converting enzyme (TACE). ADAMs-mediated shedding of cytokines such as TNF-α orchestrates immune system or inflammatory cascades and ADAMs-mediated shedding of growth factors causes cell growth or proliferation by transactivation of the growth factor receptors including epidermal growth factor receptor. Therefore, increased ADAMs-mediated shedding can induce inflammation, tissue remodeling and dysfunction associated with various cardiovascular diseases such as hypertension and atherosclerosis, and ADAMs can be a potential therapeutic target in these diseases. In this review, we focus on the role of ADAMs in cardiovascular pathophysiology and cardiovascular diseases. The main aim of this review is to stimulate new interest in this area by highlighting remarkable evidence.
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Keywords {🔍}

pubmed, article, google, scholar, cas, adam, central, biol, cell, shedding, enzyme, receptor, chem, necrosis, factor, ectodomain, growth, blobel, tumor, mol, httpsdoiorgjbcm, disintegrin, vascular, wang, cleavage, signaling, cells, res, endothelial, eguchi, metalloproteinase, sci, atherosclerosis, zhang, role, angiotensin, van, tace, biochem, adhesion, converting, activity, expression, mice, human, adams, saftig, cardiovascular, hypertension, activation,

Topics {✒️}

at1r/ros/p38 mapk/adam17 pathway releases tumour-necrosis factor-alpha tnf-alpha–converting enzyme inhibitor tnf-alpha-converting enzyme cleaves tumor necrosis factor-alpha erk/gef-h1/rhoa pathway tumour necrosis factor-alpha month download article/chapter promotes metalloproteinase-dependent cross-talk tnf-α-converting enzyme tnf-alpha converting enzyme tnf-alpha-converting enzyme severe-acute respiratory syndrome-coronavirus tgf-beta/smad3 signaling pathway l-selectin-dependent secondary capture phorbol-ester-stimulated ectodomain shedding growth factor-stimulated epithelial membrane-anchored heparin-binding egf obesity-induced insulin resistance α converting enzyme tumor necrosis factor membrane-anchored growth factor egf-receptor ligand epigen egf receptor cross-talk phorbol ester-induced shedding epidermal growth factor protease-regulated feedback loop bech-serra jj agonist-induced cardiac hypertrophy c1q-induced cell death partially l-selectin dependent high glucose requires mediates inflammation-induced shedding nf-kappab ligand tpa-induced ectodomain shedding modulating tgf-alpha availability angiotensin-converting enzyme-2 ldl-receptor deficient mice soluble m6p/igf2r released organ-specific vascular structures organ-specific vascular beds alzheimer-type cardiovascular aging multiple platelet-expressed proteinases gpcr-mediated egfr transactivation ppar-alpha activator fenofibrate hematopoietic colony-stimulating factors proinflammatory trans-signaling function polycystic kidney disease steroidal anti-inflammatory drugs post-myocardial infarction repair

Questions {❓}

Melenhorst WB, Visser L, Timmer A, van den Heuvel MC, Stegeman CA, van Goor H (2009) ADAM17 upregulation in human renal disease: a role in modulating TGF-alpha availability?

Schema {🗺️}

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         Hypertension
         Atherosclerosis
         Heart disease
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         Endothelium
         Inflammation
         Angiotensin
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         Biomedicine
         general
         Life Sciences
         Biochemistry
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