Correction: Mouse SIRT3 Attenuates Hypertrophy-Related Lipid Accumulation in the Heart through the Deacetylation of LCAD

نویسندگان

  • Tongshuai Chen
  • Junni Liu
  • Na Li
  • Shujian Wang
  • Hui Liu
  • Jingyuan Li
  • Yun Zhang
  • Peili Bu
چکیده

[This corrects the article DOI: 10.1371/journal.pone.0118909.].

برای دانلود رایگان 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

Revisiting protein acetylation and myocardial fatty acid oxidation.

In the 20th century, our knowledge of posttranslational modifications (PTMs) and their impact on protein function/enzyme activity was largely confined to that of protein phosphorylation and their regulation via kinases and phosphatases. However, as our scientific tools have become more sophisticated, and as we have advanced our knowledge of cellular/molecular biology, which has further been aug...

متن کامل

Mouse Sirt3 promotes autophagy in AngII-induced myocardial hypertrophy through the deacetylation of FoxO1

Sirt3, a mitochondrial NAD+-dependent histone deacetylase, is the only member proven to promote longevity in mammalian Sirtuin family. The processed short form of Sirt3 has been demonstrated to target many mediators of energy metabolism and mitochondrial stress adaptive program. Autophagy serves as a dynamic recycling mechanism and provides energy or metabolic substrates. Among the mechanisms t...

متن کامل

SIRT3 regulates mitochondrial fatty-acid oxidation by reversible enzyme deacetylation

Sirtuins are NAD-dependent protein deacetylases. They mediate adaptive responses to a variety of stresses, including calorie restriction and metabolic stress. Sirtuin 3 (SIRT3) is localized in the mitochondrial matrix, where it regulates the acetylation levels of metabolic enzymes, including acetyl coenzyme A synthetase 2 (refs 1, 2). Mice lacking both Sirt3 alleles appear phenotypically normal...

متن کامل

Regulation of the mPTP by SIRT3-mediated deacetylation of CypD at lysine 166 suppresses age-related cardiac hypertrophy

Cardiac failure is a leading cause of age-related death, though its root cause remains unknown. Mounting evidence implicates a decline in mitochondrial function due to increased opening of the mitochondrial permeability transition pore (mPTP). Here we report that the NAD+-dependent deacetylase SIRT3 deacetylates the regulatory component of the mPTP, cyclophilin D (CypD) on lysine 166, adjacent ...

متن کامل

Fasting-induced myocardial lipid accumulation in long-chain acyl-CoA dehydrogenase knockout mice is accompanied by impaired left ventricular function.

BACKGROUND Lipotoxicity may be a key contributor to the pathogenesis of cardiac abnormalities in mitochondrial long-chain fatty acid β-oxidation (FAO) disorders. Few data are available on myocardial lipid levels and cardiac performance in FAO deficiencies. The purpose of this animal study is to assess fasting-induced changes in cardiac morphology, function, and triglyceride (TG) storage as a co...

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

عنوان ژورنال:

دوره 10  شماره 

صفحات  -

تاریخ انتشار 2015