Autophagy is a fundamental evolutionarily conserved process where the cells degrade their own cellular material. It plays an essential role in both cellular and whole organism homeostasis. During autophagy, cytoplasmic components are sequestered into double-membrane vesicles called autophagosomes, which then fuse with lysosomes where their content is degraded. The products of degradation are transported back into the cytoplasm through lysosomal membrane permeases and can be reused by the cell. Autophagy serves as a cellular response in nutrient starvation but it is also responsible for the removal of aggregated proteins, damaged organelles and invading bacteria and viruses. Failure of autophagy to perform these functions underlies the pathogenesis of several diseases including neurodegeneration, infections and cancer.
We welcome authors to submit original research articles as well as review articles that will stimulate the continuing efforts to understand the molecular mechanisms underlying the role of autophagy in health and disease. Potential topics include, but are not limited to:
• Omics approaches to study autophagy
• Imaging approaches to study autophagy
• CRISPR/cas9 in autophagy research
• Structure of ATG proteins
• Post translational modifications of ATG proteins
• Chemical modulators of autophagy
• Transcriptional regulation of autophagy
• Physiology & mechanisms of autophagosome formation
• Autophagy in cell differentiation
• Autophagy and tissue homeostasis
• Autophagy and proteostasis
• Autophagy and ageing
• The pathophysiology of autophagy during development
• The pathophysiology of autophagy in diseases
• Stem cell biology and autophagy
• Selective autophagy (mitophagy, xenophagy, aggrephagy, lipophagy, pexophagy)
• Autophagy and model organisms
• Chaperone-mediated autophagy
• Endosomal microautophagy
Autophagy is a fundamental evolutionarily conserved process where the cells degrade their own cellular material. It plays an essential role in both cellular and whole organism homeostasis. During autophagy, cytoplasmic components are sequestered into double-membrane vesicles called autophagosomes, which then fuse with lysosomes where their content is degraded. The products of degradation are transported back into the cytoplasm through lysosomal membrane permeases and can be reused by the cell. Autophagy serves as a cellular response in nutrient starvation but it is also responsible for the removal of aggregated proteins, damaged organelles and invading bacteria and viruses. Failure of autophagy to perform these functions underlies the pathogenesis of several diseases including neurodegeneration, infections and cancer.
We welcome authors to submit original research articles as well as review articles that will stimulate the continuing efforts to understand the molecular mechanisms underlying the role of autophagy in health and disease. Potential topics include, but are not limited to:
• Omics approaches to study autophagy
• Imaging approaches to study autophagy
• CRISPR/cas9 in autophagy research
• Structure of ATG proteins
• Post translational modifications of ATG proteins
• Chemical modulators of autophagy
• Transcriptional regulation of autophagy
• Physiology & mechanisms of autophagosome formation
• Autophagy in cell differentiation
• Autophagy and tissue homeostasis
• Autophagy and proteostasis
• Autophagy and ageing
• The pathophysiology of autophagy during development
• The pathophysiology of autophagy in diseases
• Stem cell biology and autophagy
• Selective autophagy (mitophagy, xenophagy, aggrephagy, lipophagy, pexophagy)
• Autophagy and model organisms
• Chaperone-mediated autophagy
• Endosomal microautophagy
