AMPK activation, a preventive therapeutic target in the transition from cardiac injury to heart failure.

نویسندگان

  • Christophe Beauloye
  • Luc Bertrand
  • Sandrine Horman
  • Louis Hue
چکیده

Heart failure is a progressive muscular disorder leading to a deterioration of the heart characterized by a contractile dysfunction and a chronic energy deficit. As a consequence, the failing heart is unable to meet the normal metabolic and energy needs of the body. The transition between compensated left ventricular hypertrophy and the de-compensated heart is multifactorial, although metabolic disturbances are considered to play a significant role. In this respect, the AMP-activated protein kinase (AMPK) could be a potential target in heart failure development. AMPK senses the energy state of the cell and orchestrates a global metabolic response to energy deprivation. We briefly review here the current knowledge about the chronic energy deficit of the failing heart, as well as the role of AMPK in energy homeostasis and in the control of non-metabolic targets in relation to cardiac hypertrophy and heart failure. The relative importance of energetic and non-metabolic effects in the potential cardioprotective action of AMPK is discussed.

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

Effect of pre-treatment with oxytocin on cardiac enzymes in regional ischemiareperfusion injury induced in the rat heart

Introduction: Cardiac preconditioning represents the most potent and consistently reproducible method of rescuing heart tissue from undergoing irreversible ischemic damage. The aim of the present study was to evaluate oxytocin (OT) induced cardioprotection and its signaling pathways on lactate dehydrogenase (LDH) and creatine kinase-MB isoenzyme (CK-MB) in the anesthetized rats. Methods: Ei...

متن کامل

Effects of Taurine, Sestrin 2 and Phyllanthin on coronary artery diseases

Heart failure is a growing epidemic in the worldwide. Atherosclerosis is a major mechanism of cardiovascular disease including myocardial infarction and peripheral arterial disease. Moreover, it causes many diseases and deaths around the world. Atherosclerosis, like coronary artery disease (CAD), is associated with inflammation and oxidative stress. The current article has been collected the s...

متن کامل

Enhancing AMPK activation during ischemia protects the diabetic heart against reperfusion injury.

AMPK activation during ischemia helps the myocardium to cope with the deficit of energy production. As AMPK activity is considered to be impaired in diabetes, we hypothesized that enhancing AMPK activation during ischemia above physiological levels would protect the ischemic diabetic heart through AMPK activation and subsequent inhibition of mitochondrial permeability transition pore (mPTP) ope...

متن کامل

The effects of ginsenoside Rb1 on fatty acid β-oxidation, mediated by AMPK, in the failing heart

Objective(s): This study intended to investigate the effects of Ginsenoside-Rbl (Gs-Rbl) on fatty acid β-oxidation (FAO) in rat failing heart and to identify potential mechanisms of Gs-Rbl improving heart failure (HF) by FAO pathway dependent on AMP-activated protein kinase (AMPK). Materials and Methods: Rats with chronic HF, induced by adriamycin (Adr), were randomly grouped into 7 groups. Gs-...

متن کامل

A journey in doxorubicin-induced cardiotoxicity with emphasizing on the role of Connexin 43 and Sirtuin-3

Cancer has become a major health problem worldwide. The reported incidence of new cancer cases is estimated at 19.3 million, with a mortality rate of 10 million in the world in 2020. There are some approaches for cancer treatment such as chemotherapy, neoadjuant surgery, hormone therapy, and radiotherapy. Chemotherapy is an aggressive form of chemical drug therapy meant to destroy rapidly growi...

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:
  • Cardiovascular research

دوره 90 2  شماره 

صفحات  -

تاریخ انتشار 2011