In the past several years, it has been demonstrated that the reactive oxygen species (ROS) may act as intracellular signalling molecules to activate or inhibit specific signalling pathways and regulate physiological cellular functions. It is now well-established that ROS regulate autophagy, an intracellular degradation process. However, the signalling mechanisms through which ROS modulate autophagy in a regulated manner have only been minimally clarified. NADPH oxidase (Nox) enzymes are membrane-bound enzymatic complexes responsible for the dedicated generation of ROS. Different isoforms of Nox exist with different functions. Recent studies demonstrated that Nox-derived ROS can promote autophagy, with Nox2 and Nox4 representing the isoforms of Nox implicated thus far. Nox2- and Nox4-dependent autophagy plays an important role in the elimination of pathogens by phagocytes and in the regulation of vascular- and cancer-cell survival. Interestingly, we recently found that Nox is also important for autophagy regulation in cardiomyocytes. We found that Nox4, but not Nox2, promotes the activation of autophagy and survival in cardiomyocytes in response to nutrient deprivation and ischaemia through activation of the PERK (protein kinase RNA-like endoplasmic reticulum kinase) signalling pathway. In the present paper, we discuss the importance of Nox family proteins and ROS in the regulation of autophagy, with a particular focus on the role of Nox4 in the regulation of autophagy in the heart.
Skip Nav Destination
Article navigation
Review Article|
December 09 2014
Role of NADPH oxidase in the regulation of autophagy in cardiomyocytes
Sebastiano Sciarretta;
Sebastiano Sciarretta
*Department of Cell Biology and Molecular Medicine, Cardiovascular Research Institute, Rutgers New Jersey Medical School, Newark, NJ, U.S.A.
†IRCCS Neuromed, Pozzilli, IS, Italy
Search for other works by this author on:
Derek Yee;
Derek Yee
1
*Department of Cell Biology and Molecular Medicine, Cardiovascular Research Institute, Rutgers New Jersey Medical School, Newark, NJ, U.S.A.
Search for other works by this author on:
Paul Ammann;
Paul Ammann
1
*Department of Cell Biology and Molecular Medicine, Cardiovascular Research Institute, Rutgers New Jersey Medical School, Newark, NJ, U.S.A.
Search for other works by this author on:
Narayani Nagarajan;
Narayani Nagarajan
*Department of Cell Biology and Molecular Medicine, Cardiovascular Research Institute, Rutgers New Jersey Medical School, Newark, NJ, U.S.A.
Search for other works by this author on:
Massimo Volpe;
Massimo Volpe
†IRCCS Neuromed, Pozzilli, IS, Italy
‡Faculty of Medicine and Psychology, Department of Clinical and Molecular Medicine, Division of Cardiology, University “Sapienza”, Rome, Italy
Search for other works by this author on:
Giacomo Frati;
Giacomo Frati
†IRCCS Neuromed, Pozzilli, IS, Italy
§Department of Medico-Surgical Sciences and Biotechnologies, University “Sapienza”, Latina, Italy.
Search for other works by this author on:
Junichi Sadoshima
*Department of Cell Biology and Molecular Medicine, Cardiovascular Research Institute, Rutgers New Jersey Medical School, Newark, NJ, U.S.A.
Correspondence: Professor Junichi Sadoshima (email [email protected]).
Search for other works by this author on:
Publisher: Portland Press Ltd
Received:
May 29 2014
Revision Received:
October 06 2014
Accepted:
October 21 2014
Online ISSN: 1470-8736
Print ISSN: 0143-5221
© The Authors Journal compilation © 2015 Biochemical Society
2015
Clin Sci (Lond) (2015) 128 (7): 387–403.
Article history
Received:
May 29 2014
Revision Received:
October 06 2014
Accepted:
October 21 2014
Citation
Sebastiano Sciarretta, Derek Yee, Paul Ammann, Narayani Nagarajan, Massimo Volpe, Giacomo Frati, Junichi Sadoshima; Role of NADPH oxidase in the regulation of autophagy in cardiomyocytes. Clin Sci (Lond) 1 April 2015; 128 (7): 387–403. doi: https://doi.org/10.1042/CS20140336
Download citation file:
Sign in
Don't already have an account? Register
Sign in to your personal account
You could not be signed in. Please check your email address / username and password and try again.
Could not validate captcha. Please try again.
Biochemical Society Member Sign in
Sign InSign in via your Institution
Sign in via your InstitutionGet Access To This Article
Open Access for all
We offer compliant routes for all authors from 2025. With library support, there will be no author nor reader charges in 5 journals. Check here |
![]() |