Inflammation, Oxidative Stress and Protein Aggregation; Any Links?
A special issue of Cells (ISSN 2073-4409).
Deadline for manuscript submissions: closed (15 October 2019) | Viewed by 21352
Special Issue Editors
2. Jožef Stefan International Postgraduate School, 1000 Ljubljana, Slovenia
Interests: mechanisms of protein folding and aggregation, amyloid metal interaction, amyloid-membrane interaction; amyloid pore formation; lipid composition modulation of protein aggregation; proteomics and bioinformatics; interactomes and protein function annotation
Special Issues, Collections and Topics in MDPI journals
Interests: protein folding; protein aggregation; protein design; high-throughput screening; bioinformatics; amyloids; Parkinson; nanomaterials; phase separation; prions; drug discovery
Special Issues, Collections and Topics in MDPI journals
Interests: innate immune response; inflammasome; mitochondria; oxidative stress; proteinases and inhibitors
Special Issues, Collections and Topics in MDPI journals
Special Issue Information
Dear Colleagues,
Inflammation is a complex immune response that enables survival during infection and maintains tissue homeostasis. In response to pathogens, damaged cells, or irritants a cascade of signals leads to the recruitment of immune cells. The sustained robust inflammation may lead to serious disorders due to the overproduction of pro-inflammatory cytokines and tissue damage. The proinflammatory cytokines IL-1β and IL-18 play a crucial role in tissue homeostasis. Their secretion is determined by the inflammasome, a multicomponent complex that processes IL-1β and IL-18 into mature cytokines. Reactive oxygen species (ROS) are implicated in inflammasome activation.
Proteostasis (proportion between the synthesis, translation, folding and degradation of proteins) should be in balance in a healthy cell, including neurons. However, due to different stressors among them, heat (fever, infection), acidification (lack or excess of nutrients) and oxidative stress, the mis-folding and aggregation of otherwise normal sequences of proteins occurs. Different chaperones, i.e., heat shock proteins, are turned on to deaggregate and restore the folding of proteins, however, the degradation and clearance from the cell by autophagy happen as a last resource. ROS can also increase upon protein aggregation, due to metals binding to the aggregates, membrane perturbation or permeabilization by soluble aggregates.
In this Special Issue we propose: 1) to discuss how oxidative stress influences the inflammatory immune response; 2) studies of the regulatory pathways, which are turned on in the cytosol to restore proteostasis; and 3) studies which shed light on the connections between different stressors and the amount of protein aggregates, and the localization of the smallest, still soluble aggregates (oligomers), which are supposed to be the most toxic.
Overall, by means of the proposed Special Issue, we expect to come closer to understanding the links between inflammatory response, oxidative stress and protein aggregation. Such knowledge may lead to common therapeutic targets to fight decreased proteostasis in aging or in neurodegenerative diseases.
Prof. Dr. Eva Žerovnik
Prof. Dr. Salvador Ventura
Dr. Nataša Kopitar Jerala
Guest Editors
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Keywords
- inflammation
- cytokines IL-1β and IL-18
- reactive oxygen species (ROS)
- protein mis-folding
- protein aggregation
- amyloid
- amyloid-beta peptide
- neurodegeneration
- signalling pathways
- autophagy
- mitochondrial damage
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