Relevant bibliographies by topics / Endothelin converting enzyme 1

Academic literature on the topic 'Endothelin converting enzyme 1'

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Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "Endothelin converting enzyme 1"

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Cottrell, Graeme S., Benjamin E. Padilla, Silvia Amadesi, Daniel P. Poole, Jane E. Murphy, Markus Hardt, Dirk Roosterman, Martin Steinhoff, and Nigel W. Bunnett. "Endosomal Endothelin-converting Enzyme-1." Journal of Biological Chemistry 284, no. 33 (June 16, 2009): 22411–25. http://dx.doi.org/10.1074/jbc.m109.026674.

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Barnes, K., K. Shimada, M. Takahashi, K. Tanzawa, and A. J. Turner. "Metallopeptidase inhibitors induce an up-regulation of endothelin-converting enzyme levels and its redistribution from the plasma membrane to an intracellular compartment." Journal of Cell Science 109, no. 5 (May 1, 1996): 919–28. http://dx.doi.org/10.1242/jcs.109.5.919.

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Endothelin-converting enzyme is a phosphoramidon-sensitive membrane metallopeptidase that catalyses the final step in biosynthesis of the potent vasoactive endothelin peptides. Immunomagnetic separation technology and immunohistochemistry have been used to demonstrate the co-localisation of endothelin-converting enzyme with the established ectoenzyme, aminopeptidase N, on the surface of endothelial cells. Unlike aminopeptidase N, however, endothelin-converting enzyme is seen to associate in clusters on the plasma membrane which can be distinguished from caveolae both biochemically and immunologically. Pre-treatment of endothelial cells with the metallopeptidase inhibitors phosphoramidon or thiorphan in the range 0.01-100 microM produced a dose-dependent increase in the levels of endothelin-converting enzyme protein and its accumulation in an intracellular compartment. No corresponding change in the levels of endothelin-converting enzyme-1 mRNA was detected under these conditions, nor in the levels of the closely related metalloenzyme, endopeptidase-24.11. The phosphoramidon and thiorphan-dependent increase is not due to direct inhibition of endothelin-converting enzyme not endopeptidase-24.11 but, rather, to an inhibition of the selective turnover of endothelin-converting enzyme protein.
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Wu, Ching-Fang, Ching-Tai Lee, Yao-Hung Kuo, Tzu-Haw Chen, Chi-Yang Chang, I.-Wei Chang, and Wen-Lun Wang. "High endothelin-converting enzyme-1 expression independently predicts poor survival of patients with esophageal squamous cell carcinoma." Tumor Biology 39, no. 9 (September 2017): 101042831772592. http://dx.doi.org/10.1177/1010428317725922.

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Patients with esophageal squamous cell carcinoma have poor survival and high recurrence rate, thus an effective prognostic biomarker is needed. Endothelin-converting enzyme-1 is responsible for biosynthesis of endothelin-1, which promotes growth and invasion of human cancers. The role of endothelin-converting enzyme-1 in esophageal squamous cell carcinoma is still unknown. Therefore, this study investigated the significance of endothelin-converting enzyme-1 expression in esophageal squamous cell carcinoma clinically. We enrolled patients with esophageal squamous cell carcinoma who provided pretreated tumor tissues. Tumor endothelin-converting enzyme-1 expression was evaluated by immunohistochemistry and was defined as either low or high expression. Then we evaluated whether tumor endothelin-converting enzyme-1 expression had any association with clinicopathological findings or predicted survival of patients with esophageal squamous cell carcinoma. Overall, 54 of 99 patients with esophageal squamous cell carcinoma had high tumor endothelin-converting enzyme-1 expression, which was significantly associated with lymph node metastasis ( p = 0.04). In addition, tumor endothelin-converting enzyme-1 expression independently predicted survival of patients with esophageal squamous cell carcinoma, and the 5-year survival was poorer in patients with high tumor endothelin-converting enzyme-1 expression ( p = 0.016). Among patients with locally advanced and potentially resectable esophageal squamous cell carcinoma (stage II and III), 5-year survival was poorer with high tumor endothelin-converting enzyme-1 expression ( p = 0.003). High tumor endothelin-converting enzyme-1 expression also significantly predicted poorer survival of patients in this population. In patients with esophageal squamous cell carcinoma, high tumor endothelin-converting enzyme-1 expression might indicate high tumor invasive property. Therefore, tumor endothelin-converting enzyme-1 expression could be a good biomarker to identify patients with worse survival and higher risks of recurrence, who might benefit from the treatment by endothelin-converting enzyme-1 inhibitor.
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D'Orléans-Juste, P., M. Plante, J. C. Honoré, E. Carrier, and J. Labonté. "Synthesis and degradation of endothelin-1." Canadian Journal of Physiology and Pharmacology 81, no. 6 (June 1, 2003): 503–10. http://dx.doi.org/10.1139/y03-032.

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The endothelin-converting enzyme (ECE) is the main enzyme responsible for the genesis of the potent pressor peptide endothelin-1 (ET-1). It is suggested that the ECE is pivotal in the genesis of ET-1, considering that the knockout of both genes generates the same lethal developments during the embryonic stage. Several isoforms of the ECE have been disclosed, namely ECE-1, ECE-2, and ECE-3. Within each of the first two groups, several sub-isoforms derived through splicing of single genes have also been identified. In this review, the characteristics of each sub-isoform for ECE-1 and 2 will be discussed. It is important to mention that the ECE is, however, not the sole enzyme involved in the genesis of endothelins. Indeed, other moieties, such as chymase and matrix metalloproteinase II, have been suggested to be involved in the production of ET intermediates, such as ET-1 (1–31) and ET-1 (1–32), respectively. Other enzymes, such as the neutral endopeptidase 24–11, is curiously not only involved in the degradation and inactivation of ET-1, but is also responsible for the final production of the peptide via the hydrolysis of ET-1 (1–31). In this review, we will attempt to summarize, through the above-mentioned characteristics, the current wisdom on the role of these different enzymes in the genesis and termination of effect of the most potent pressor peptide reported to date.Key words: endothelin converting enzyme, endothelin-1, isoforms, human, inhibitors, chymase, ET-1 (1–31).
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Pupilli, C., P. Romagnani, L. Lasagni, F. Bellini, N. Misciglia, N. Emoto, M. Yanagisawa, M. Rizzo, M. Mannelli, and M. Serio. "Localization of endothelin-converting enzyme-1 in human kidney." American Journal of Physiology-Renal Physiology 273, no. 5 (November 1, 1997): F749—F756. http://dx.doi.org/10.1152/ajprenal.1997.273.5.f749.

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The distribution of endothelin-converting enzyme-1 (ECE-1) mRNA and protein was investigated in human kidney excised because of renal tumors. ECE-1 immunoreactivity was detected by immunohistochemistry throughout the different areas of the kidney in the vascular and tubular structures. In the cortex, ECE-1 immunostaining was present in the endothelial surface of arcuate and interlobular arteries and in arterioles. Weak specific immunoreactivity was present over some proximal and distal tubules. Few endothelial glomerular cells contained ECE-1 protein. In the medulla, ECE-1 immunoreactivity was observed in the vasa recta bundles and capillaries. ECE-1 immunostaining was also detected in the outer and inner medullary collecting ducts and thin limbs of Henle’s loops. Immunohistochemical detection of the von Willebrand factor on adjacent sections confirmed the endothelial nature of the vascular cells that exhibited ECE-1 immunostaining. The distribution patterns of ECE-1 mRNA, investigated by in situ hybridization, appeared similar to that obtained by immunohistochemistry in the cortical and medullary vasculature and in different portions of the nephron. Northern blot and densitometric analyses demonstrated that ECE-1 mRNA levels were quantitatively similar in both the renal cortex and medulla. These results demonstrate that vascular endothelial and tubular epithelial cells in the cortex and medulla of the human kidney synthesize ECE-1, which, in turn, may play an important role in regulating endothelin production in physiological and pathological conditions.
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Jafri, Farahdiba, and Adviye Ergul. "Nuclear Localization of Endothelin-Converting Enzyme-1." Arteriosclerosis, Thrombosis, and Vascular Biology 23, no. 12 (December 2003): 2192–96. http://dx.doi.org/10.1161/01.atv.0000099787.21778.55.

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Tapia, Julio C., and Ignacio Niechi. "Endothelin-converting enzyme-1 in cancer aggressiveness." Cancer Letters 452 (June 2019): 152–57. http://dx.doi.org/10.1016/j.canlet.2019.03.033.

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Kuruppu, Sanjaya, and A. Ian Smith. "Endothelin Converting Enzyme-1 phosphorylation and trafficking." FEBS Letters 586, no. 16 (June 21, 2012): 2212–17. http://dx.doi.org/10.1016/j.febslet.2012.06.020.

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Lin, J., and C. Wei. "Enhancement of Endothelin Converting Enzyme and Endothelin Receptor Subtypes in Human Myocardium with Congestive Heart Failure." Microscopy and Microanalysis 6, S2 (August 2000): 608–9. http://dx.doi.org/10.1017/s1431927600035534.

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Endothelin-1 (ET-1) is a potent endothelial cell-drived vasoconstrictive peptide which is increased in congestive heart failure (CHF). ET-1 is converted from its precursor big ET-1 by activation of endothelin converting enzyme (ECE). ET-1 binding to ET-A receptor in vascular smooth muscle cells stimulates vasoconstriction and binding to ET-B receptor in vascular endothelial cells mediates vasodilation. In previous studies, we and others demonstrated that plasma ET-1 was significantly increased in congestive heart failure. However, the presentation and localization of endothelin converting enzyme and endothelin receptors (ET-A and ET-B) in human cardiac tissue with and without heart failure remain unclear. Therefore, the current study was designed to investigate the expression and localization of endothelin receptors and endothelin converting enzyme in human myocardium in the absence or presence of congestive heart failure.Human atrial tissues (n=6) were obtained from normal subjects and end-stage CHF patients during cardiac transplantation. The expression of ECE, ET-A and ET-B were determined by immunohistochemical staining (IHCS).
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Kido-Nakahara, Makiko, Jörg Buddenkotte, Cordula Kempkes, Akihiko Ikoma, Ferda Cevikbas, Tasuku Akiyama, Frank Nunes, et al. "Neural peptidase endothelin-converting enzyme 1 regulates endothelin 1–induced pruritus." Journal of Clinical Investigation 124, no. 6 (May 8, 2014): 2683–95. http://dx.doi.org/10.1172/jci67323.

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Dissertations / Theses on the topic "Endothelin converting enzyme 1"

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Park, Sung-Hae 1971. "Role of endothelin-1 and endothelin converting enzyme-1 in bleomycin-induced pulmonary fibrosis in rats." Thesis, McGill University, 1996. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=24032.

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Idiopathic pulmonary fibrosis (IPF) belongs to the group of the interstitial lung diseases and is characterized by inflammation, proliferation of fibroblasts and type II pneumocytes, and increased collagen deposition. Inflammatory cells, by releasing mediators and cytokines, participate in the pathogenesis of IPF. Endothelin-1 (ET-1), a vasoconstrictor and mitogenic peptide, is one of the mediators that has been shown to be involved in the fibrotic process of IPF in humans. There are, however, no studies examining the role of ET-1 in animal models of IPF. We used the rat model of pulmonary fibrosis, induced by bleomycin, to study the role of ET-1 and endothelin converting enzyme-1 (ECE-1) in IPF using immunohistochemistry (IHC). We also studied by morphometry the effect of bosentan, the mixed ET-A/B receptor antagonist, on the severity of the fibrosis. We found increased ET-1 and ECE-1 immunoreactivities in the lungs of the fibrosis group compared with the control group (P $<$ 0.05), principally in epithelial cells. By morphometry, we found a decrease in the volume fraction (Vv) of air and an increase in the Vv of connective tissue in the fibrosis group compared with control. The fibrosis was significantly reduced by bosentan (P $<$ 0.05). These results are consistent with the notion that ET-1 is an important mediator of bleomycin-induced pulmonary fibrosis.
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Baluyut, Crystal. "Characterization of human endothelin converting enzyme (ECE-1) promoter diversity in vasular endothelial cells." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape10/PQDD_0010/MQ40767.pdf.

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Kido, Tsuneo. "Processing of proendothelin-1 at the carboxyl-terminus of big endothelin-1 is essential for proteolysis by endothelin-converting enzyme-1 in vivo." Kyoto University, 1997. http://hdl.handle.net/2433/202209.

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Kaburagi, Satoshi. "The role of endothelin-converting enzyme-1 in the development of α1-adrenergic-stimulated hypertrophy in cultured neonatal rat cardiac myocytes." Kyoto University, 2001. http://hdl.handle.net/2433/150597.

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Masatsugu, Ken. "Shear stress attenuates endothelin and endothelin-converting enzyme expression through oxidative stress." Kyoto University, 2004. http://hdl.handle.net/2433/147555.

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Hasegawa, Hiroshi. "Purification of a novel endothelin-converting enzyme specific for big endothelin-3." Kyoto University, 1998. http://hdl.handle.net/2433/182268.

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Harrison, Vanessa Jane. "The characterisation of endothelin-converting enzyme in endothelial cells." Thesis, Queen Mary, University of London, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.307673.

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Ikura, Takeshi. "cDNA cloning and expression of bovine endothelin converting enzyme." Kyoto University, 1997. http://hdl.handle.net/2433/202206.

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Govender, Ureshnie. "The characterisation of RAS converting enzyme 1 activity and regulation." Thesis, Queen's University Belfast, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.527705.

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Hocharoen, Lalintip. "Catalytic Metallopeptide Promoted Inactivation of Enzyme Targets Related to Disease: Angiotensin Converting Enzyme-1 and SortaseA." The Ohio State University, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=osu1354634371.

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Books on the topic "Endothelin converting enzyme 1"

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Baluyut, Crystal. Characterization of human endothelin converting enzyme (ECE-1) promoter diversity in vasular endothelial cells. Ottawa: National Library of Canada, 1998.

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Dhaun, Neeraj, and David J. Webb. Endothelins and their antagonists in chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0114_update_001.

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The endothelins (ETs) are a family of related peptides of which ET-1 is the most powerful endogenous vasoconstrictor and the predominant isoform in the cardiovascular and renal systems. The ET system has been widely implicated in both cardiovascular disease and chronic kidney disease (CKD). ET-1 contributes to the pathogenesis and maintenance of hypertension and arterial stiffness, as well endothelial dysfunction and atherosclerosis. By reversal of these effects, ET antagonists, particularly those that block ETA receptors, may reduce cardiovascular risk. In CKD patients, antagonism of the ET system may be of benefit in improving renal haemodynamics and reducing proteinuria, effects seen both in animal models and in some human studies. Data suggest a synergistic role for ET receptor antagonists with angiotensin-converting enzyme inhibitors in lowering blood pressure, reducing proteinuria, and in animal models in slowing CKD progression. However, in clinical trials, fluid retention or cardiac failure has caused concern and these agents are not yet ready for general use for risk reduction in CKD.
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Dilsizian, Vasken, Ines Valenta, and Thomas H. Schindler. Myocardial Viability Assessment. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199392094.003.0021.

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Heart failure may be a consequence of ischemic or non-ischemic cardiomyopathy. Etiologies for LV systolic dysfunction in ischemic cardiomyopathy include; 1) transmural scar, 2) nontransmural scar, 3) repetitive myocardial stunning, 4) hibernating myocardium, and 5) remodeled myocardium. The LV remodeling process, which is activated by the renin-angiotensin system (RAS), stimulates toxic catecholamine actions and matrix metalloproteinases, resulting in maladaptive cellular and molecular alterations5, with a final pathway to interstitial fibrosis. These responses to LV dysfunction and interstitial fibrosis lead to progressive worsening of LV function. Established treatment options for ischemic cardiomyopathy include medical therapy, revascularization, and cardiac transplantation. While there has been continuous progress in the medical treatment of heart failure with beta-blockers, angiotensin-converting enzyme (ACE) inhibition, angiotensin II type 1 receptor (AT1R) blockers, and aldosterone to beneficially influence morbidity and mortality, the 5-years mortality rate for heart failure patients remains as high as 50%. Revascularization procedures include percutaneous transluminal coronary artery interventions (PCI) including angioplasty and endovascular stent placement and coronary artery bypass grafting (CABG). Whereas patents with heart failure due to non-coronary etiologies may best benefit from medical therapy or heart transplantation, coronary revascularization has the potential to improve ventricular function, symptoms, and long term survival, in patients with heart failure symptoms due to CAD and ischemic cardiomyopathy.
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Lai, Kar Neng, and Sydney C. W. Tang. Immunoglobulin A nephropathy. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0068_update_001.

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Immunoglobulin A nephropathy is characteristically slowly evolving, and studies from autopsies and kidney donors show that deposition of immunoglobulin A is quite common and not necessarily associated with overt disease. However, series of biopsy-diagnosed patients that extend to 20 or 30 years report rates of end-stage renal failure of up to 40–50%. A very approximate overall rate of end-stage renal disease of 1% per year has been suggested. Proteinuria, glomerular filtration rate (GFR), and possibly some features on renal biopsies enable risk stratification, but all patients need long-term monitoring. Treatment is based on the use of angiotensin converting-enzyme inhibitors for patients with proteinuria, and blood pressure control, and of course during most of the previous long-term studies patients would not have been treated with these agents or to modern blood pressure standards. For patients who show loss of GFR despite this, or other markers of high risk, the best evidence is for treatment with high-dose corticosteroids over a limited period of months. There is little convincing evidence for additional benefit from cytotoxic or other immunomodulatory agents, except possibly in the most aggressive disease, when there is weak evidence for cyclophosphamide. Some studies claim benefit from tonsillectomy, but this is not clear, and most nephrologists only recommend this for patients with recurrent tonsillitis.
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Lynch, Bernadette, and Aine Burns. The patient with scleroderma. Edited by Giuseppe Remuzzi. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0165.

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Scleroderma is tightness, thickening, and non-pitting induration of skin. Two forms of the skin disease are described. Limited cutaneous systemic sclerosis (lcSSc) which occurs distal to the wrists (or ankles) and/or over the face and neck, often associated with longstanding Raynaud’s phenomenon, and diffuse cutaneous systemic sclerosis (dcSSc) where truncal as well as acral skin involvement occurs as well as tendon friction rubs. In this latter condition the onset of the skin changes occurs within 1 year of onset of Raynaud’s phenomenon; however, the skin involvement may precede onset of vascular symptoms.The skin manifestations are the outward manifestation of a systemic disease, systemic sclerosis. Lung, heart, and gut involvement are frequent. Scleroderma renal crisis, usually presenting as accelerated hypertension and acute kidney injury, is one of the most severe complications of this disease. Autoantibodies against RNA polymerase are associated with scleroderma renal crisis. It occurs in 12% of dcSSc and 2% of lcSSc patients (men and women) and carries a high morbidity and mortality although careful supportive care and blood pressure management using angiotensin converting enzyme inhibitors (ACEI) or angiotensin-II receptor blockers have improved short-term outcomes. In general, beta blockers should be avoided in the early management.Approximately two-thirds of patients require dialysis, of these many recover enough function to come off dialysis. Higher blood pressure and younger age at presentation have a better prognosis. ACEIs should be continued even after dialysis is established as the latter increases the chance of late recovery. Average time to coming off dialysis is 11 months but recovery is uncommon after 24 months. After a crisis renal function continues to improve for several years.
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Gnudi, Luigi, Giorgio Gentile, and Piero Ruggenenti. The patient with diabetes mellitus. Edited by Giuseppe Remuzzi. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0149_update_001.

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About one third of patients with type 1 diabetes develop diabetic nephropathy long-term (usually not before at least 10 years of diabetes), though this proportion is falling as standards of care have risen. Nephropathy is strongly associated with other microvascular complications of diabetes, so that some degree of retinopathy is to be expected, and evidence of neuropathy is common. Patients with type 2 diabetes are equally susceptible, but this is an older group in which vascular disease and other pathologies are also more likely. The rise in type 2 diabetes accounts for diabetes being the most common recorded cause of end stage renal disease (ESRD) in the developed world.Diabetic nephropathy is characterized by a progression through hyperfiltration, microalbuminuria, hypertension, overt proteinuria, nephrotic syndrome, loss of GFR, to ESRD. Risk factors for developing it include genetic factors (though no major single gene effects have been identified), and quality of glycaemic control.The risk of progression can at early stages be reduced by improved glycaemic control, and control of hypertension also slows progression. However angiotensin converting enzyme inhibitors or receptor blockers (ACEi, ARB) are the standard of care for patients with microalbuminuria or overt proteinuria, as they have been shown to reduce the risk of renal endpoints. Combination therapy with both ACEi and ARB together has been associated with a high risk of AKI, hyperkalaemia and other adverse effects so is not generally recommended. Other promising agents in combination are under investigation but none adequately proven at this stage.Patients who reach ESRD have reduced survival on all modalities compared to age-matched patients with other diagnoses. Best rehabilitation and survival for those who are suitable is through renal transplantation, though combined pancreas-renal transplantation may offer still better outcomes for selected patients.
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Ferro, Charles J., and Khai Ping Ng. Recommendations for management of high renal risk chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0099.

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Poorer renal function is associated with increasing morbidity and mortality. In the wider population this is mainly as a consequence of cardiovascular disease. Renal patients are more likely to progress to end-stage renal disease, but also have high cardiovascular risk. Aiming to reduce both progression of renal impairment and cardiovascular disease are not contradictory. Focusing on the management of high-risk patients with proteinuria and reduced glomerular filtration rates, it is recommended that blood pressure should be kept below 140/90, or 130/80 if proteinuria is > 1 g/24 h (protein:creatinine ratio (PCR) >100 mg/mmol or 0.9 g/g). These targets may be modified according to age and other factors. Angiotensin-converting enzyme inhibitors (ACEIs) or angiotensin receptor antagonists should form part of the therapy for patients with proteinuria > 0.5 g/24 h (PCR > 50 mg/mmol or 0.45 g/g). Use of ACEIs or angiotensin receptor blockers in patients with lower levels of proteinuria may be indicated in some patient groups even in the absence of hypertension, notably in diabetic nephropathy. Evidence that other agents that reduce proteinuria bring additional benefits is weak at present. The best studies of ‘dual-blockade’ with various combinations of ACEIs, ARBs, and renin inhibitors have shown additional hazard with little evidence of additional benefit. Hyperlipidaemia—regardless of lipid levels, statin therapy is indicated in secondary cardiovascular prevention, and in primary prevention where cardiovascular risk is high, noting that current risk estimation tools do not adequately account for the increased risk of patients with CKD. There is not substantial evidence that lipid lowering therapy impacts on average rates of loss of GFR in progressive CKD. Non-drug lifestyle interventions to reduce cardiovascular risk, including stopping smoking, are important for all. Acidosis—in more advanced CKD it is justified to treat acidosis with oral sodium bicarbonate. Diet—sodium restriction to < 100 mmol/day (6 g/day) and avoidance of excessive dietary protein are justified in early to moderate CKD. Recommendations to limit levels of protein to 0.8 g/kg body weight are suggested by some, but additional protective effects of this are likely to be slight in patients who are otherwise well managed. Low-protein diets may carry some risk. Lower-protein diets may however be used to prevent symptoms in advanced CKD not treated by dialysis.
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Book chapters on the topic "Endothelin converting enzyme 1"

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Schomburg, Dietmar, and Dörte Stephan. "Endothelin-converting enzyme 1." In Enzyme Handbook 16, 501–4. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-642-58903-4_93.

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Takayanagi, Ryoichi, Keizo Ohnaka, Wei Liu, Takeshi Ito, and Hajime Nawata. "Molecular Biology of Endothelin-Converting Enzyme (ECE)." In Endothelin, 75–92. Totowa, NJ: Humana Press, 1998. http://dx.doi.org/10.1007/978-1-4757-2783-8_3.

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Oparil, Suzanne, Qingcheng Meng, Shuang-dan Sun, Yiu-Fai Chen, and Louis J. Dell’Italia. "Tissue Angiotensin Converting Enzyme." In Vascular Endothelium, 205–39. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4613-0355-8_15.

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D’Orléans-Juste, Pedro, and Sabine Télémaque. "Pharmacology of the Human Precursors of Endothelin: Role of Functional Receptors and Endothelin-Converting Enzyme." In Membrane Physiopathology, 207–26. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2616-2_13.

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Zimmermann, M., C. Jung, A. Raabe, O. Spanehl, and V. Seifert. "Effect of Endothelin-Converting Enzyme Inhibitors on big Endothelin-1 Induced Contraction of Rabbit Basilar Artery." In Cerebral Vasospasm, 73–75. Vienna: Springer Vienna, 2001. http://dx.doi.org/10.1007/978-3-7091-6232-3_16.

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Berg, Kåre. "Insertion/Deletion (I/D) Polymorphism in the Angiotensin Converting Enzyme (ACE) Gene." In Vascular Endothelium, 57–73. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4899-0133-0_6.

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Orfanos, S. E., A. Kotanidou, and C. Roussos. "Pulmonary Endothelial Angiotensin Converting Enzyme Activity in Lung Injury." In Intensive Care Medicine, 100–110. New York, NY: Springer New York, 2002. http://dx.doi.org/10.1007/978-1-4757-5551-0_9.

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Orfanos, S. E., X.-L. Chen, J. W. Ryan, A. Y. K. Chung, S. E. Burch, and J. D. Catravas. "Assay of Pulmonary Microvascular Endothelial Angiotensin Converting Enzyme, in Vivo: Comparison of Three Methods." In Vascular Endothelium, 192–93. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-2437-3_41.

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Papapetropoulos, Andreas, S. E. Burch, Stavros Topouzis, and John D. Catravas. "Radiation-Induced Alteration in Angiotensin Converting Enzyme Activity in Cultured Bovine Pulmonary Artery Endothelial Cells." In Vascular Endothelium, 194. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-2437-3_42.

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Armaganidis, A., S. E. Orfanos, D. Sfyras, P. Kaltsas, J. D. Catravas, J. Economidou, and Ch Roussos. "Effect of Extracorporeal CO2 Removal on Pulmonary Capillary Endothelium-Bound Angiotensin Converting Enzyme Activity in the Human." In Vascular Endothelium, 237–38. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4899-0133-0_17.

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Conference papers on the topic "Endothelin converting enzyme 1"

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Belles, Mary Elizabeth, Meena Halaka, Jessica M. Do, Parth Majmudar, Reem Sidani, Hannah Stephen, Molly Watson, and Rebecca E. Conway. "Abstract A58: Expression and function of endothelin converting enzyme 1 and endothelin receptors in breast cancer invasion." In Abstracts: AACR Special Conference: Advances in Breast Cancer; October 17-20, 2015; Bellevue, WA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1557-3125.advbc15-a58.

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Baudin, B., L. Drouet, J. L. Carrier, M. Bérard, and Q. Y. Wu. "DISTRIBUTION OF ENDOTHELIAL MARKERS ALONG THE VASCULAR TREE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643357.

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Few specific markers of the endothelial cells are available. Von Willebrand factor has been recognized as the most specific but we have shown that its intracellular content and extracellular release varies largely along the vascular tree of the pig. Synthesis is maximal in capillaries and in pulmonary artery endothelial cells. Synthesis is almost nil in the aorta. Intermediary values are encountered in the inferior vena cava. We studied the distribution of angiotensin converting enzyme (ACE) in endothelial cells along the vascular tree, as synthesis, storage, membrane expression and release of this enzyme is totally different from that of von Willebrand factor. Primary culture of endothelial cells from various origin of the vascular tree were studied. ACE was assessed by a functional radiometric assay using a specific substrate, cellular expression depends : 1 - on culture conditions (medium with serum, adult pig serum, foetal calf serum, medium without serum), 2 - on time in culture and 3 - on the degree of cellular confluency. ACE is easily measured both in cellular extract and in the medium. After cellular fractionation, ACE is concentrated in membrane fractions. Changes were found between the arterial and venous endothelial cells but no significant variation in the distribution between intracellular and released ACE were noted. Arterial endothelium (aortic and pulmonary artery) behaved similarly while in venous endothelium (inferior vena cava) both the cellular and the releasable ACE decreased. A specific antibody to the cellular form of the porcine ACE is being raised to complete these functional studies by antigenic dosages and immunolocalization.
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Peters, Dorothea M., Bhola K. Dahal, Djuro Kosanovic, Daniela Haag, Susan Wehner, Rio Dumitrascu, Josef Messinger, et al. "The Dual Neutral Endopeptidase/Endothelin Converting Enzyme Inhibitor SLV338 Inhibits Experimental Pulmonary Hypertension In Rats." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a6439.

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ITO, KATSUTOSHI, KENTARO OHWAKI, HIDETOSHI ARAKAWA, and MASAKO MAEDA. "DEVELOPMENT OF TANDEM BIOLUMINESCENT ENZYME IMMUNOASSAY FOR ANGIOTENSIN I AND ENDOTHELIN-1." In Proceedings of the 13th International Symposium. WORLD SCIENTIFIC, 2005. http://dx.doi.org/10.1142/9789812702203_0112.

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Saldeen, K., R. Moalli, and T. Saldeen. "EFFECT OF A FIBRIN-DERIVED PEPTIDE ON PULMONARY ANGIOTENSIN CONVERTING ENZYME (ACE) ACTIVITY AND ON PRESSURE RESPONSES TO BRADYKININ (BK)." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644331.

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Decreased ACE activity is a common finding in patients with adult respiratory distress syndrome (ARDS) and in animal models of lung injury. The nature of this effect is unknown. Fibrin, also a common finding in lung injury, is degraded to small peptides by proteolytic enzymes. Peptide 6A, corresponding to amino acid residues 43-47 of the BB-chain of fibrin (cgen), is produced by plasmin degradation of fibrin and has been shown to inhibit ACE in vitro. The purpose of the present investigation was to study whether peptide 6A inhibits pulmonary ACE in vivo and, if so, determine its effect of hemodynamic changes induced by bradykinin (BK) in the rabbit. We investigated the effect of peptide 6A an the hydrolysis of a synthetic ACE substrate, benzoyl-phe-ala-pro (BPAP) in anesthetized rabbits and in isolated lungs. Peptide 6A caused a reversible, dose-dependent inhibition of BPAP hydrolysis. The ID 50 for peptide 6A inhibition of ACE hydrolysis of BPAP was approximately 1 micrcmole.In both isolated rabbit lupgp and in the intact animal, BK injection elicited a dose dependent increase in pulmonary arterial pressure. In intact animals, this was accompanied by a dose dependent decrease in systemic arterial pressure.In both preparations, responses to BK were potentiated by addition of 1 micromole of peptide 6A. In isolated lungs, co-injection of peptide 6A significantly increased the pulmonary artery pressure response to every dose of BK except the highest (1 mg). In the anesthetized rabbit, 1 micromole of peptide 6A significantly (p<0.05) increased the pulmonary hypertensive response to 100 and 200 nanograms of BK and significantly (p<0.05) decreased the systemic hypotensive response following 100 , 200 , 300 and 400 nanograms of BK. The amount of BK needed to increase pulmonary arterial pressure was 1000-fold greater in the isolated lungs than in the intact animals. Peptides of this type might contribute to decreased ACE activity in patients with ARDS and may potentiate BK induced pulmonary hypertension and systemic hypotension in these patients.
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Gause, S., M. L. Ribeiro Neto, and D. A. Culver. "Assessing the Clinical Utility of Serum Angiotensin-Converting Enzyme, Soluble IL-2 Receptor, and 1-25 Vitamin D in the Diagnosis of Extra-Pulmonary Sarcoidosis." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a4309.

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Surya, I. E., and J. W. N. Akkerman. "HUMAN PLASMA PAF-ACETYLHYDROLASE, NORMALLY PRESENT IN LOW DENSITY LIPOPROTEINS, IS ASSOCIATED WITH HIGH DENSITY LIPOPROTEINS IN A PATIENT WITH LDL DEFICIENCY." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642882.

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Platelet Activating Factor (l-0-alkyl-2-acetyl-sn-glycerol-3-phosphocholine; PAF) plays an important role in allergic and inflammatory reactions and activates platelets in the nanomolar range. One of the main factors that controls PAF activity in blood is an enzyme that hydrolyzes the acetyl-chain thereby converting PAF to biologically inactive lyso-PAF. The enzyme is acid labile and normally associated with apo B-containing low density lipoproteins (LDL, density 1,006-1,063 g/ml).We investigated whether a deficiency in LDL would affect the enzyme activity. PAF-inactivating activity was measured in plasma from a patient with abetalipoproteinemia, a rare autosomal recessive disorder, characterized by the absence of apo B and apo B-containing lipoproteins (chylomicrons, VLDL and LDL). Plasma triglyceride was 0,2 mmol/1 (normal 1,40-2,20 mmol/1) and cholesterol 1,3 mmol/1 (normal 5,60-7,70 mmol/1). Separation of lipoproteins by density gradient centrifugation revealed a slightly decreased HDL content whereas VLDL and LDL were below the detection limit (0,20 mmol/1; based on cholesterol content).Despite the absence of LDL, PAF-inactivating activity in plasma of the patient (measured by (1) the decrease in aggregation inducing activity of PAF after incubation, (ii) the conversion of 3H-acyl-PAF to lysa PAF, separated on TLC, (iii) the liberation of 3H-label from 3H-acetyl PAF) was present and even slightly higher than in normal plasma (hydrolysis of 3 3H-PAF after 20 minutes incubation was 78 ± 4% and 65 ± 6% in patient and normals, respectively, n = 4). Subfractionation revealed that the enzyme activity was present in fractions with densities of 1,065-1,214 g/ml, which are typical for HDL.These results indicate that PAF-acetylhydrolase, although normally present in LDL, binds to HDL in a patient with extreme LDL-deficiency.Supported by the Dutch Heart Foundation (grant 85082)
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Jacobs, M., L. Lahousse, H. P. Van Eeckhoutte, S. R. A. Wijnant, J. R. Delanghe, G. G. Brusselle, and K. R. Bracke. "Effect of ACE1 (Angiotensin Converting Enzyme 1) Polymorphism Rs1799752 on Protein Levels of ACE2, the SARS-CoV-2 (Severe Acute Respiratory Syndrome Coronavirus 2) Entry Receptor, in Alveolar Lung Epithelium." In American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a1272.

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Westwood, Brian M., Hossam A. Shaltout, and Mark C. Chappell. "Modeling of Angiotensin Peptide Metabolism in Renal Proximal Tubules." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-190990.

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The recent discovery of angiotensin converting enzyme 2 (ACE2) as a functional peptidase within the renin-angiotensin system (RAS) has added a new layer of complexity to the enzymatic cascade of this hormonal system. ACE2 is highly expressed in the proximal tubules of the kidney, an important tissue site involved in blood pressure regulation. Therefore, we derived a model for the processing of Ang I which is the immediate precursor to the biologically active peptides Ang II and Ang-(1-7) based on metabolism data in isolated proximal tubules of the sheep kidney (1). Given the individual experimental velocities for several peptidases expressed in the proximal tubules including ACE, ACE2 and neprilysin, rate constants were calculated to describe the conservation equations for the processing of Ang I, Ang II and Ang-(1-7) We modeled the system with Ang I as the initial substrate and peptide concentrations for the downstream products were calculated using Euler’s method.
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Bruyakin, S. D., and D. A. Makarevich. "MODELING OF POTENTIAL PROTEIN S1 SARS-COV-2 LIGANDS." In SAKHAROV READINGS 2021: ENVIRONMENTAL PROBLEMS OF THE XXI CENTURY. International Sakharov Environmental Institute of Belarusian State University, 2021. http://dx.doi.org/10.46646/sakh-2021-2-27-30.

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The S1 protein of SARS-CoV-2 (hereinafter referred to as the S1 protein) is probably the main factor in the pathogenesis of COVID-19. In our opinion, the elimination or decrease in the concentration of this protein will reduce the inflammatory process and, accordingly, damage to organs and tissues by the activated immune system. An analysis of the complexes of the Angiotensin-converting enzyme 2 (ACE2) and the S1 protein (ACE2-S1) will determine the oligopeptides that are ligands for binding the S1 protein, the timely removal of which from the blood of patients with COVID-19 will prevent the development of severe multi-organ complications. Besides, the immobilized oligopeptide that binds the S1 protein will be able to remove from the body viral particles located in the extracellular space [1].
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Reports on the topic "Endothelin converting enzyme 1"

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Wu, Xiaoqi, Jisen Zhao, Maoxia Fan, and Dongo Guo. Quality of Evidence Supporting the Effects of Xinmailong injection in Heart Failure: An Overview of Systematic Reviews and Meta-Analyses. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, October 2022. http://dx.doi.org/10.37766/inplasy2022.10.0023.

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Review question / Objective: 2.1.1 type of research SRs/MAs of RCT (randomized controlled trial) of Xinmailong injection for the treatment of heart failure. 2.1.2 Subject investigated All included patients met internationally recognized diagnostic criteria for heart failure.There are no limitations on age, gender, ethnicity, time of onset, source of cases and language of publication. 2.1.3 Type of Intervention The control group was treated with conventional basic Western medicine recommended by the guidelines related to heart failure[1, 11], including antiplatelet drugs, anticoagulants, vasodilators, beta-blockers,ACEI (angiotensin-converting enzyme inhibitors), lipid-lowering drugs, and diuretic agents. and other drug treatment. The intervention group was given Xinmailong injection on the basis of the control group.
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