Hepatic Steatosis in ACE2-Deficient Mice

نویسندگان

  • Valéria Nunes-Souza
  • Natalia Alenina
  • Fatimunnisa Qadri
  • Josef M. Penninger
  • Robson Augusto S. Santos
  • Michael Bader
  • Luiza A. Rabelo
  • Swaran J. S. Flora
چکیده

1Max Delbrück Center for Molecular Medicine, Berlin, Germany 2Laboratório de Reatividade Cardiovascular (LRC), Núcleo de Sı́ndromeMetabólica, Universidade Federal de Alagoas, Maceió, Brazil 3National Institute of Science and Technology in Nano-Biopharmaceutics (N-BIOFAR), Belo Horizonte, Brazil 4Departamento de Fisiologia e Farmacologia, Centro de Biociências (CB), Universidade Federal de Pernambuco, Recife, Brazil 5Universidade Federal de Minas Gerais, Belo Horizonte, Brazil 6Institute of Molecular Biotechnology of the Austrian Academy of Sciences, Vienna, Austria 7Charité–University Medicine Berlin, Berlin, Germany 8Institute for Biology, University of Lübeck, Lübeck, Germany 9German Center for Cardiovascular Research (DZHK), Berlin, Germany

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

CD36/Sirtuin 1 Axis Impairment Contributes to Hepatic Steatosis in ACE2-Deficient Mice

Background and Aims. Angiotensin converting enzyme 2 (ACE2) is an important component of the renin-angiotensin system. Since angiotensin peptides have been shown to be involved in hepatic steatosis, we aimed to evaluate the hepatic lipid profile in ACE2-deficient (ACE2-/y) mice. Methods. Male C57BL/6 and ACE2-/y mice were analyzed at the age of 3 and 6 months for alterations in the lipid profil...

متن کامل

Angiotensin-converting enzyme 2/angiotensin-(1–7)/Mas axis activates Akt signaling to ameliorate hepatic steatosis

The classical axis of renin-angiotensin system (RAS), angiotensin (Ang)-converting enzyme (ACE)/Ang II/AT1, contributes to the development of non-alcoholic fatty liver disease (NAFLD). However, the role of bypass axis of RAS (Angiotensin-converting enzyme 2 (ACE2)/Ang-(1-7)/Mas) in hepatic steatosis is still unclear. Here we showed that deletion of ACE2 aggravates liver steatosis, which is corr...

متن کامل

Allantoin improves methionine-choline deficient diet-induced nonalcoholic steatohepatitis in mice through involvement in endoplasmic reticulum stress and hepatocytes apoptosis-related genes expressions

Objective(s): Non-alcoholic steatohepatitis (NASH) is defined by steatosis and inflammation in the hepatocytes, which can progress to cirrhosis and possibly hepatocellular carcinoma. However, current treatments are not entirely effective. Allantoin is one of the principal compounds in many plants and an imidazoline I receptor agonist as well. Allantoin has positive eff...

متن کامل

Pioglitazone Upregulates Angiotensin Converting Enzyme 2 Expression in Insulin-Sensitive Tissues in Rats with High-Fat Diet-Induced Nonalcoholic Steatohepatitis

BACKGROUND AND AIM Thiazolidinediones (TZDs) can improve hepatic steatosis in nonalcoholic steatohepatitis (NASH). Angiotensin (Ang) II, the primary effector of renin-angiotensin system (RAS), plays vital roles in the development and progression of NASH. And some AngII-mediated effects can be regulated by TZDs. Angiotensin-converting enzyme (ACE) 2, a new component of RAS, can degrade Ang II to...

متن کامل

Hepatic Deficiency of Augmenter of Liver Regeneration Exacerbates Alcohol-Induced Liver Injury and Promotes Fibrosis in Mice

Why only a subpopulation (about 15%) of humans develops liver cirrhosis due to alcohol is a critical as yet unanswered question. Liver-specific depletion of augmenter of liver regeneration (ALR) protein in mice causes robust steatosis and hepatocyte apoptosis by 2 weeks; these pathologies regress subsequently with return of ALR expression even at lower than control levels, but the mice develop ...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:

دوره   شماره 

صفحات  -

تاریخ انتشار 2016