Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.23.15 (renin)
 35,795 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Non-alcoholic fatty liver disease (NAFLD) is now the commonest cause of chronic liver disease in developed countries. Treatment depends on the stage of disease, and non-invasive methods for risk stratification are urgently needed. Lifestyle modification (aimed at weight loss and increasing physical activity) and management of the features of metabolic syndrome are vital for all patients with NAFLD. Metformin is the first-line therapy for diabetic patients with NAFLD and also reduces the risk of hepatocellular carcinoma. Clinicians should have a low threshold for introducing a statin for the management of dyslipidaemia. Antihypertensive agents that target the renin-angiotensin system should be first-line in NAFLD for the management of hypertension. For patients with progressive disease, liver-directed pharmacotherapy with vitamin E should be considered. Non-alcoholic steatohepatitis cirrhosis is an increasingly common indication for liver transplantation.
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PMID:Treatment of non-alcoholic fatty liver disease. 2503 93

Non-alcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver disease in developed countries and it is now considered a risk factor for cardiovascular disease. Evidence linking NAFLD to the development and progression of chronic kidney disease (CKD) is emerging as a popular area of scientific interest. The rise in simultaneous liver-kidney transplantation as well as the significant cost associated with the presence of chronic kidney disease in the NAFLD population make this entity a worthwhile target for screening and therapeutic intervention. While several cross-sectional and case control studies have been published to substantiate these theories, very little data exists on the underlying cause of NAFLD and CKD. In this review, we will discuss the most recent publications on the diagnosis of NAFLD as well new evidence regarding the pathophysiology of NAFLD and CKD as an inflammatory disorder. These mechanisms include the role of obesity, the renin-angiotensin system, and dysregulation of fructose metabolism and lipogenesis in the development of both disorders. Further investigation of these pathways may lead to novel therapies that aim to target the NAFLD and CKD. However, more prospective studies that include information on both renal and liver histology will be necessary in order to understand the relationship between these diseases.
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PMID:NAFLD and Chronic Kidney Disease. 2708 31

Non-alcoholic fatty liver disease (NAFLD) is becoming the most common chronic liver disease. NAFLD may evolve to non-alcoholic steatohepatitis (NASH), which is causally related to cirrhosis and cardiovascular disease (CVD) mortality. There is no generally accepted effective treatment for NAFLD/NASH. Chronic kidney disease (CKD) is relatively common and might co-exist with NAFLD/NASH, aggravate one another, and increase CVD risk. Common therapies could improve outcome. Potent statins at high doses, such as atorvastatin and rosuvastatin, ameliorate NAFLD/NASH and reduce the mortality rates by half as compared with those on the same statins but without liver disease and CVD-related events are reduced by atorvastatin for patients with all stages of CKD. The new anti-diabetic medication classes, the sodium-glucose co-transporter-2 inhibitors (SGLT2i) and the glucagon like peptide receptor agonists (GLP1 RA) for patients with NAFLD/NASH, CKD and T2DM are useful because they ameliorate NAFLD/NASH, delay the evolution of CKD, and substantially reduce CVD and all-cause mortality. Thus, the common use of high potency statins, renin-angiotensin-aldosterone system inhibitors, and the newer anti-diabetic agents increase compliance and can substantially reduce CVD risk and the rate of liver and kidney adverse events, improving quality of life and survival.
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PMID:The Co-Existence of NASH and Chronic Kidney Disease Boosts Cardiovascular Risk: Are there any Common Therapeutic Options? 2867 27

Sarcopenia associated with chronic liver disease (CLD) is one of the more common extrahepatic features in patients with these pathologies. Among the cellular alterations observed in the muscle tissue under CLD is the decline in the muscle strength and function, as well as the increased fatigue. Morphological changes, such as a decrease in the fiber diameter and transition in the fiber type, are also reported. At the molecular level, sarcopenia for CLD is characterized by: i) a decrease in the sarcomeric protein, such as myosin heavy chain (MHC); ii) an increase in the ubiquitin-proteasome system markers, such as atrogin-1/MAFbx1 and MuRF-1/TRIM63; iii) an increase in autophagy markers, such as LC3II/LC3I ratio. Among the regulators of muscle mass is the renin-angiotensin system (RAS). The non-classical axis of RAS includes the Angiotensin 1-7 [Ang-(1-7)] peptide and its receptor Mas, which in skeletal muscle has anti-atrophic effect in models of muscle wasting induced by immobilization, lipopolysaccharide, myostatin or angiotensin II. In this paper, we evaluated the effect of Ang-(1-7) on the sarcopenia by CLD in a murine model induced by the 5-diethoxycarbonyl-1,4-dihydrocollidine (DDC) hepatotoxin administered through diet. Our results show that Ang-(1-7) administration prevented the decline of the function and strength of muscle and increased the fatigue detected in the DDC-fed mice. Besides, we observed that the decreased fiber diameter and MHC levels, as well as the transition of fiber types, were all abolished by Ang-(1-7) in mice fed with DDC. Finally, Ang-(1-7) can decrease the atrogin-1 and MuRF-1 expression as well as the autophagy marker in mice treated with DDC. Together, our data support the protective role of Ang-(1-7) on the sarcopenia by CLD in mice.
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PMID:Protective Effect of Angiotensin 1-7 on Sarcopenia Induced by Chronic Liver Disease in Mice. 3248 91

In chronic liver disease, the incidence of cirrhosis is increasing. About 1 million deaths from cirrhosis are reported annually by WHO, occupying the 11th position in the hierarchy of pathologies that cause death (1). The prevalence of cirrhosis is often underestimated based on the fact that one third of the patients are asymptomatic (2). Regardless of whether it is elective or urgent extra-hepatic surgery, operative interventions in this range of patients are burdened by an increased risk of perioperative morbidity and mortality (3,4). This reality requires the evaluation of the benefit-risk balance for each patient with the surgical firm indication. A journal of the medical literature, presented over the period 1995-2018 (PubMed), noted that the most frequent extrahepatic interventions in the cirrhotic patient were addressed to the cholecyst and CBD (23%), parietal defects (hernias, events) in 17 %, gastric pathology (19%) and rectum-colon (19%).v Liver cirrhosis is frequently associated with abnormalities of coagulation mechanisms: thrombopenia and platelet dysfunctions, decreased coagulation factors but also proteins involved in fibrinolysis. Cardio-circulatory changes are all the more important as the cirrhotic pathology is more evolved, being expressed by hyperkinetic syndrome and systemic vasodilation with hyper-flow, tachycardia and low peripheral resistance (5). The "trigger" element of these anomalies is the portal hypertension and the porto-systemic shunts that involve vasodilating mediators but also the compensatory activation of the renin-angiotensin system (6). The perioperative anaesthetic strategy in the patients is integrated in a multidisciplinary effort of specific management.
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PMID:Digestive Surgery at the Cirrhotic Patient. 3311 87

The emergence of coronavirus disease-2019 induced by a newly identified b-coronavirus, namely severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has constituted a public health emergency. Even though it was considered a zoonotic disease, the virus has also spread among humans via respiratory secretions. The expression and distribution of angiotensin converting enzyme type 2 (ACE2) in various human organs might also show other possible infection routes. High ACE2 ribonucleic acid expression has been identified in the gastrointestinal tract (GI) indicating its importance as a possible infection pathway of SARS-CoV-2. ACE2 induces viral entry into the host and most importantly has been found to be associated with the function of the gut. Its deficiency has been implicated in several pathologies such as colorectal inflammation. The renin-angiotensin system (RAS) is an essential regulatory cascade operating both at a local tissue level and at the systemic or circulatory level. The RAS may be important in the pathogenesis of chronic liver disease and is associated with the up-regulation of ACE2. Thus, the aim of this review is firstly, the analysis of some important general and genome characteristics of SARS-CoV-2 and secondly, and most importantly, to focus on the utility of ACE2 receptors in both SARS-CoV-2 replication and pathogenesis, especially in the GI tract.
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PMID:Origin and genomic characteristics of SARS-CoV-2 and its interaction with angiotensin converting enzyme type 2 receptors, focusing on the gastrointestinal tract. 3324 96


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