Ang-(1-7) treatment attenuates lipopolysaccharide-induced early pulmonary fibrosis.
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It is suggested that AngII and AT1R levels exhibit opposite dynamic trends during LPS-induced early pulmonary fibrosis, as do Ang-(1-7) and Mas.About:
This article is published in Laboratory Investigation.The article was published on 2019-07-05 and is currently open access. It has received 25 citations till now. The article focuses on the topics: Pulmonary fibrosis & ARDS.read more
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Potential harmful effects of discontinuing ACE-inhibitors and ARBs in COVID-19 patients.
TL;DR: Therapeutic considerations how to increase soluble ACE-2 in plasma in order forACE-2 to capture and thereby inactivate SARS-CoV-2 are proposed and discussed.
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Renin-Angiotensin System: An Important Player in the Pathogenesis of Acute Respiratory Distress Syndrome.
TL;DR: Targeting the renin–angiotensin system and reducing the pathogen’s cell entry could be a promising therapeutic strategy in the struggle against COVID-19.
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Pterostilbene prevents LPS-induced early pulmonary fibrosis by suppressing oxidative stress, inflammation and apoptosis in vivo.
TL;DR: In this paper, the effects of Pterostilbene (Pts) on early pulmonary fibrosis were investigated in mice treated with LPS, and the results showed that LPS injection triggered the production of myeloperoxidase (MPO) and malondialdehyde (MDA) and the depletion of superoxide dismutase (SOD) and glutathione (GSH), and that these effects were notably reversed by treatment with Pts.
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"A Chain Only as Strong as Its Weakest Link": An Up-to-Date Literature Review on the Bidirectional Interaction of Pulmonary Fibrosis and COVID-19.
Radu Crisan-Dabija,Cristina Alice Pavel,Iolanda Valentina Popa,Andrei Tarus,Alexandru Burlacu +4 more
TL;DR: It is found that there is a complexity of interactions between coexisting idiopathic pulmonary fibrosis/interstitial lung disease (ILD) and COVID-19 disease, and patients recovering from severe COVID -19 disease are at serious risk of developing PF.
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Pharmacotherapy in COVID-19 patients: a review of ACE2-raising drugs and their clinical safety.
Saghir Akhtar,Ibrahim F. Benter,Mohammed Danjuma,Mohammed Danjuma,Suhail A.R. Doi,Syed Shahzad Hasan,Abdella M. Habib +6 more
TL;DR: Books suggests that ACEIs/ARBs usage generally appears to be clinically safe though their use in severe COVID-19 patients might increase the risk of acute renal injury, and further clinical and mechanistic studies are needed in assessing the safety of all classes of ACE2 raising medications.
References
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Epithelial-mesenchymal transition and its implications for fibrosis.
Raghu Kalluri,Eric G. Neilson +1 more
TL;DR: This review highlights recent advances in the process of EMT signaling in health and disease and how it may be attenuated or reversed by selective cytokines and growth factors.
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Src protein-tyrosine kinase structure and regulation.
TL;DR: Protein-tyrosine phosphatases such as PTPalpha displace phosphotyrosine 527 from the Src SH2 domain and mediate its dephosphorylation leading to Src kinase activation, which results in inhibition from phosphorylation by C-terminal SRC kinase.
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Angiotensin-converting enzyme 2, angiotensin-(1-7) and Mas: new players of the renin-angiotensin system
TL;DR: Recent findings related to the biological role of the ACE2/Ang-(1-7)/Mas arm in the cardiovascular and renal systems, as well as in metabolism are discussed.
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ACE2, angiotensin-(1-7) and Mas receptor axis in inflammation and fibrosis
TL;DR: The role of the ACE2/Ang‐(1‐7)/Mas axis in modifying processes associated with acute and chronic inflammation, including leukocyte influx, fibrogenesis and proliferation of certain cell types is focused on.
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The renin-angiotensin-aldosterone system: a specific target for hypertension management
Matthew R. Weir,Victor J. Dzau +1 more
TL;DR: Modification of angiotensin II effect may serve a dual purpose, as blood pressure reduction will occur with less stretch, stress, and turbulence of the vascular wall, but there will also be less stimulation for restructuring and remodeling of the cardiovascular tree.