Complex diseases are caused by a combination of genetic, environmental, and lifestyle factors. Many degenerative, metabolic, inflammatory diseases, cancers, and infections are included in this group of entities. Autophagy is known to be dysregulated in these pathological situations, some of them related to aging. Multiple different functions of the autophagy pathway or specific autophagy proteins are likely to be contributory in novel therapeutic, diagnostic, or preventative strategies. Autophagy is a cellular catabolic process that sequesters and delivers cytoplasmic components to the lysosome for degradation. There are three main forms of autophagy: (1) micro-autophagy refers to the direct sequestration of cytosolic components by the lysosome; (2) the chaperon mediated autophagy involves the translocation of specific proteins across the lysosome membrane through the receptor LAMP2A; and (3) macroautophagy, where cargoes are sequestered within a unique double-membrane vesicle called autophagosome, which fuses with the lysosome to deliver the inner vesicle in the degradative compartment.
By recycling cytoplasmic constituents, autophagy controls cellular bioenergetics and tissue remodeling. In addition, autophagy allows the selective elimination of misfolded proteins, proteins aggregates, damaged organelles, intracellular pathogens, and lipid droplets. This pathway is called selective autophagy and has high relevance in the cell response to disease. Independently of the lysosomal degradation, the autophagic machinery can be involved in other non-degradative processes, such as the unconventional secretion by secretory autophagy, the mechanism of phagocytosis, and the regulation of inflammatory signaling. As a result of the broad range of cellular functions, selective and secretory autophagy pathways, as well as autophagic proteins, play a key role in aging and have been linked to a wide range of cancers, infections, neurodegenerative disorders, metabolic diseases, inflammatory diseases, and muscle diseases.
This Topic seeks to unravel mechanisms, allowing autophagy to prevent or treat different complex diseases. For example, lifestyle and nutritional factors, such as exercise and caloric restriction, may exert their known health benefits through the autophagy pathway. Several currently available drugs have been shown to enhance autophagy, and this action may be repurposed for use in novel clinical indications. The development of new drugs, more selective inducers of autophagy, or the designing of precise strategies against autophagic molecules are expected to maximize clinical benefits while minimizing toxicity. This Research Topic will cover current approaches on degradative or non-degradative autophagy pathways and molecules that could be target for prevention or treatment of acute and complex disease.
We welcome the submission of Original Research articles, Methods, Reviews and Mini-Review articles. Areas to be covered may include, but are not limited to, the following topics:
- New models for the study of degradative and non-degradative autophagic pathways or ATG genes in human complex diseases and aging such as diabetes; neurodegenerative disease; imflammatory response and cancer; isquemic diseases;
- Molecular mechanisms of autophagy or ATG genes in selective and/or secretory autophagy in complex human diseases.
- Strategies and approaches for therapeutically targeting these mechanisms to improve clinal outcomes;
- Development of secretory autophagy modulators as novel therapeutic agents in inflammatory, degenerative and metabolic diseases;
- Autophagy pathways and roles of ATG genes in microbial pathophysiology, with particular interests in emerging viral pathogens such as coronaviruses.
Complex diseases are caused by a combination of genetic, environmental, and lifestyle factors. Many degenerative, metabolic, inflammatory diseases, cancers, and infections are included in this group of entities. Autophagy is known to be dysregulated in these pathological situations, some of them related to aging. Multiple different functions of the autophagy pathway or specific autophagy proteins are likely to be contributory in novel therapeutic, diagnostic, or preventative strategies. Autophagy is a cellular catabolic process that sequesters and delivers cytoplasmic components to the lysosome for degradation. There are three main forms of autophagy: (1) micro-autophagy refers to the direct sequestration of cytosolic components by the lysosome; (2) the chaperon mediated autophagy involves the translocation of specific proteins across the lysosome membrane through the receptor LAMP2A; and (3) macroautophagy, where cargoes are sequestered within a unique double-membrane vesicle called autophagosome, which fuses with the lysosome to deliver the inner vesicle in the degradative compartment.
By recycling cytoplasmic constituents, autophagy controls cellular bioenergetics and tissue remodeling. In addition, autophagy allows the selective elimination of misfolded proteins, proteins aggregates, damaged organelles, intracellular pathogens, and lipid droplets. This pathway is called selective autophagy and has high relevance in the cell response to disease. Independently of the lysosomal degradation, the autophagic machinery can be involved in other non-degradative processes, such as the unconventional secretion by secretory autophagy, the mechanism of phagocytosis, and the regulation of inflammatory signaling. As a result of the broad range of cellular functions, selective and secretory autophagy pathways, as well as autophagic proteins, play a key role in aging and have been linked to a wide range of cancers, infections, neurodegenerative disorders, metabolic diseases, inflammatory diseases, and muscle diseases.
This Topic seeks to unravel mechanisms, allowing autophagy to prevent or treat different complex diseases. For example, lifestyle and nutritional factors, such as exercise and caloric restriction, may exert their known health benefits through the autophagy pathway. Several currently available drugs have been shown to enhance autophagy, and this action may be repurposed for use in novel clinical indications. The development of new drugs, more selective inducers of autophagy, or the designing of precise strategies against autophagic molecules are expected to maximize clinical benefits while minimizing toxicity. This Research Topic will cover current approaches on degradative or non-degradative autophagy pathways and molecules that could be target for prevention or treatment of acute and complex disease.
We welcome the submission of Original Research articles, Methods, Reviews and Mini-Review articles. Areas to be covered may include, but are not limited to, the following topics:
- New models for the study of degradative and non-degradative autophagic pathways or ATG genes in human complex diseases and aging such as diabetes; neurodegenerative disease; imflammatory response and cancer; isquemic diseases;
- Molecular mechanisms of autophagy or ATG genes in selective and/or secretory autophagy in complex human diseases.
- Strategies and approaches for therapeutically targeting these mechanisms to improve clinal outcomes;
- Development of secretory autophagy modulators as novel therapeutic agents in inflammatory, degenerative and metabolic diseases;
- Autophagy pathways and roles of ATG genes in microbial pathophysiology, with particular interests in emerging viral pathogens such as coronaviruses.
