About this Research Topic
Autophagy is an essential recycling process for the elimination of multiple cellular components. Initially, it was considered a bulk, non-selective process, but now it has been characterized as a highly regulated and specific degradation pathway for removal of damaged and/or unnecessary organelles. Based on the degraded cell components, different types of selective autophagy can be identified (mitophagy, ribophagy, reticulophagy, lysophagy, pexophagy, aggrephagy, lipophagy, and glycophagy). Recent studies have revealed an intrinsic connection between selective autophagy and human diseases including inflammation, neurodegenerative disorders and cancer. However, understanding of the molecular mechanisms that regulate selective autophagy and their role in the pathogenesis of diseases is only in its early stage.
Selective autophagy can have both protective and injurious effects in human diseases, hence acting as a double-edged-sword. In our Research Topic, we are aiming to get insight into the mechanisms linking genetic or acquired defects in selective autophagy to human pathologies. Targeting in selective organellar autophagy is best analyzed in the clearance of mitochondria (mitophagy) and protein aggregates (aggrephagy). For example, recent studies have suggested that functional loss of mitophagy regulators is closely linked to cancer development, and progression or stimulation of aggrephagy might be a beneficial approach in neurodegeneration. Unraveling the molecular mechanisms that regulate selective autophagy is crucial to better define the pathogenesis of these diseases and is even more important to serve as a therapeutic target in order to counteract or defect malignancy. Knowing the signaling pathways and molecules involved will allow researchers to design more specific chemical compounds or to adapt already approved drugs to this purpose.
When considering selective autophagy, there are 3 crucial questions to be addressed:
1) how are structures or organelles selectively targeted for removal?
2) how is selective autophagy regulated independently of bulk autophagy?
3) how are genetic or acquired defects in selective autophagy linked to human diseases?
We encourage papers on several aspects relevant to selective autophagy (e.g. transcriptional and post-translational regulation, interplay with other cellular pathways – metabolism, proliferation, organelle biogenesis - , techniques and cellular/organism models to study selective autophagy, etc.). We hope this will provide new links to our current understanding of selective autophagy molecular mechanisms, with the aim to shed light on its implications in various human diseases, making it a target of future research. We will also welcome research manuscripts that propose new therapeutic approaches that target the molecular mechanisms underpinning selective autophagy in order to counteract diseases. In particular, we are interested in the use or development of chemicals that specifically affect a defined aspect of selective autophagy, rather than having a broad effect on the macro-autophagy machinery.
Authors are welcome to submit a wide range of article types including Original Research, Opinions or Reviews in order to bring novelties and new ideas to the attention of the scientific community.
Selective autophagy can have both protective and injurious effects in human diseases, hence acting as a double-edged-sword. In our Research Topic, we are aiming to get insight into the mechanisms linking genetic or acquired defects in selective autophagy to human pathologies. Targeting in selective organellar autophagy is best analyzed in the clearance of mitochondria (mitophagy) and protein aggregates (aggrephagy). For example, recent studies have suggested that functional loss of mitophagy regulators is closely linked to cancer development, and progression or stimulation of aggrephagy might be a beneficial approach in neurodegeneration. Unraveling the molecular mechanisms that regulate selective autophagy is crucial to better define the pathogenesis of these diseases and is even more important to serve as a therapeutic target in order to counteract or defect malignancy. Knowing the signaling pathways and molecules involved will allow researchers to design more specific chemical compounds or to adapt already approved drugs to this purpose.
When considering selective autophagy, there are 3 crucial questions to be addressed:
1) how are structures or organelles selectively targeted for removal?
2) how is selective autophagy regulated independently of bulk autophagy?
3) how are genetic or acquired defects in selective autophagy linked to human diseases?
We encourage papers on several aspects relevant to selective autophagy (e.g. transcriptional and post-translational regulation, interplay with other cellular pathways – metabolism, proliferation, organelle biogenesis - , techniques and cellular/organism models to study selective autophagy, etc.). We hope this will provide new links to our current understanding of selective autophagy molecular mechanisms, with the aim to shed light on its implications in various human diseases, making it a target of future research. We will also welcome research manuscripts that propose new therapeutic approaches that target the molecular mechanisms underpinning selective autophagy in order to counteract diseases. In particular, we are interested in the use or development of chemicals that specifically affect a defined aspect of selective autophagy, rather than having a broad effect on the macro-autophagy machinery.
Authors are welcome to submit a wide range of article types including Original Research, Opinions or Reviews in order to bring novelties and new ideas to the attention of the scientific community.
Keywords: Selective Autophagy, Cancer, Neurodegeneration, Autophagy, Mechanistic Studies
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
