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Protective Autophagy in Disease Prevention and Cellular Senescence

Call for Papers

In eukaryotes, autophagy is an evolutionary highly conserved degradation process. Its fundamental role is to clean up the cell by removing unnecessary, defective, or aggregated intracellular components, including soluble macromolecules (e.g., nucleic acids, proteins, carbohydrates, and lipids) and dysfunctional organelles (e.g., mitochondria, ribosomes, peroxisomes, and endoplasmic reticulum) by directing them to the lysosomes for their eventual degradation and recycling. Additionally, cells make use of autophagy in order to keep metabolic activity at the level that meets their energy requirements. The form of autophagy known as xenophagy is vitally important for removal of intracellular parasites (microbes, protozoa).

Autophagy is controlled by upstream cellular sensors such as mTOR complex 1 (to monitor availability of amino acids) and AMPK (to control energy loss), while the autophagy related genes (ATGs) are needed for the correct orchestration of the autophagy process. Moreover, recent evidence demonstrates that intracellular Ca2+ signaling plays an important role in the regulation of various steps of the process.

Growing evidence points to autophagy as playing a protective role against detrimental consequences of lesions elicited by various stimuli as misfolded proteins and distressed mitochondria. In postmitotic cells (neurons, muscle fibers, and cardiac myocytes), the accumulation of molecular lesions leads to aggregation of macromolecules and accelerated formation of lipofuscin. Impaired autophagy in the elderly exacerbates intracellular accumulation of endogenous substances and neuronal loss and limits the cellular mechanisms of adaptation to injury. Beside, autophagy is an important player in disease development caused by the excessive formation of reactive oxygen species (ROS) generated in endoplasmic reticulum and mitochondria. Autophagy might control the ROS formation and pathogenesis of diseases such as Parkinson’s and Alzheimer’s disease, atherosclerosis, cardiomyopathy, hypertension, and diabetes mellitus. This special issue aims to highlight the role of autophagy in disease. More detailed knowledge about the role, regulation, and position of autophagy in disease pathogenesis and cellular senescence would provide potential new strategies for disease prevention and management.

We would like to invite authors to contribute original research articles as well as review articles that will explore and help to understand the various roles of autophagy in disease.

Particular interest will be given to papers describing the molecular mechanisms of action by which autophagy protects from harmful effects elicited by injurious factors.

Potential topics include but are not limited to the following:

  • Autophagy control of cell senescence
  • Oxidative/endoplasmic reticulum stress and autophagy (dys)regulation
  • Autophagy in prevention of metaplasia
  • Autophagy induced by natural compounds in different cancer diseases
  • Autophagy in cancer stem cells
  • Antimicrobial effects of autophagy
  • Antiparasitic effects of autophagy
  • Mitophagy and mitochondrial dysfunctions in neurodegenerative diseases
  • Modulation of autophagy as strategy in disease prevention and cellular senescence

Authors can submit their manuscripts through the Manuscript Tracking System at

Manuscript DueFriday, 29 September 2017
First Round of ReviewsFriday, 22 December 2017
Publication DateFriday, 16 February 2018

Lead Guest Editor

Guest Editors