Autophagy and Inflammasome
A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Autophagy".
Deadline for manuscript submissions: 20 October 2024 | Viewed by 544
Special Issue Editor
Interests: innate immune response; inflammasome; mitochondria; oxidative stress; proteinases and inhibitors
Special Issues, Collections and Topics in MDPI journals
Special Issue Information
Dear Colleagues,
The NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome is a multi-protein complex that can be activated by a variety of pathogen-associated molecular patterns (PAMPS) or (DAMPS) damage-associated molecular patterns. The recognition of PAMPs or DAMPs leads to the formation of the inflammasome complex, the activation of caspase-1, the maturation of pro-inflammatory cytokines and the induction of pyroptotic cell death. Numerous studies have demonstrated the importance of NLRP3 inflammasome activation in metabolic disease and the development of diseases such as gout, type 2 diabetes, obesity, cancer, and neurodegenerative and cardiovascular disorders.
Macroautophagy (hereafter autophagy) is a cellular process that plays a critical role in maintaining cellular homeostasis by degrading and recycling intracellular components. During autophagy, cytoplasmic constituents and organelles are targeted to autophagosomes and lysosomes for degradation. Autophagy plays an important role in some inflammatory diseases associated with NLRP3 inflammasome and understanding the inter regulation between these two biological processes is necessary to comprehend the biological mechanisms and designing possible treatments for several inflammatory diseases.
This Special Issue welcomes submissions on autophagy and inflammasome activation in the regulation of immune cell function, metabolism and stress responses and diseases.
Relevant topics include, but are not limited to, the following:
- Molecular mechanisms of autophagy and inflammasome activation;
- Mitochondrial homeostasis;
- Organelle turnover;
- autophagy and mitophagy;
- Chronic inflammation;
- Cancer;
- Neurodegeneration;
- NLRP3 inflammasome;
- Infection;
- Intracellular pathogens;
- Metabolic syndrome;
- Autophagic cell death;
- Aging.
Dr. Nataša Kopitar Jerala
Guest Editor
Manuscript Submission Information
Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.
Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.
Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.
Keywords
- autophagy
- inflammasome
- immune response inflammasome
- mitochondrial ROS
- myeloid cells
- mTOR signaling
