Regular ArticleRelease and Degradation of Angiotensin I and Angiotensin II from Angiotensinogen by Neutrophil Serine Proteinases
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Targeting Neprilysin (NEP) pathways: A potential new hope to defeat COVID-19 ghost
2020, Biochemical PharmacologyCitation Excerpt :Cathepsin G was reported to be one of the neutrophil-derived serine proteases that is abundantly found in the azurophil granules and known to degrade both Angiotensinogen and Ang I into Ang II [209,210]. So far, NEP can additionally take a part in decreasing the pro-inflammatory, oxidative and pro-fibrotic effects of Ang II by minimizing the release of cathepsin G and consequently, its action on Ang I [211–213]. As NEP was reported to have more catalytic activity than ACE-2 in cleaving Ang I into Ang (1–7), it could also effectively enhance the protective activities associated with Ang (1–7) in the lung [214].
Pathophysiological role of osteopontin and angiotensin II in atherosclerosis
2016, Biochemical and Biophysical Research CommunicationsCitation Excerpt :Ang II/AT1 signaling pathway leads to an increase in cytokine and chemokine expression, including monocyte chemoattractant protein-1 (MCP-1), IL-6, IL-18, TNF-α and IL-1β [54–57] and so on. Inflammatory cells then have an endogenous RAAS that can produce Ang II, which results in a positive feedback response, perpetuating the inflammatory cycle [58–60]. Mazzolai et al. [53] demonstrated that endogenous Ang II contributes to the modification of stable plaques into a vulnerable lesions for the first time.
Myeloblastin
2013, Handbook of Proteolytic EnzymesRegulation of the renin-angiotensin system (RAS) in BeWo and HTR-8/SVneo trophoblast cell lines
2012, PlacentaCitation Excerpt :This probably accounts for the greater production of Ang 1-7 by BeWo cells compared to HTR-8/SVneo cells (Fig. 5). An alternative Aogen processing enzyme may also have been present in the culture medium, such as chymase or cathepsin D [29–31]. The latter is less likely, as it is inactive at neutral pH [30].
Complementary effects of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers in slowing the progression of chronic kidney disease
2009, American Heart JournalCitation Excerpt :However, studies have shown that levels of circulating AII return to pretreatment levels in patients receiving long-term ACEI therapy. This process, known as ACE escape, is attributed to alternate pathways for AII, such as those involving cathepsin G and elastase, which may directly convert angiotensinogen to AII, and chymases and cathepsin G, which may convert AI to AII.33-37 On the other hand, ARBs selectively block AII binding at the AT1 receptor without interfering with AII binding to AT2 receptors, thereby, allowing potentially beneficial AT2-mediated effects (vasodilation, inhibition of cell growth, improved endothelial function, and inhibition of collagen deposition).32
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