Special Issue "Mechanisms of Inflammasome Activation"
A special issue of Cells (ISSN 2073-4409).
Deadline for manuscript submissions: 1 August 2019.
We are putting together a Special Issue of Cells looking at mechanisms of inflammasome regulation, which we hope will include world-class articles on current developments in our understanding of how different inflammasomes are regulated and their importance in health and disease. We welcome contributions, as review articles or original research papers, on this ever-expanding field of research. In particular, recent advancements in our understanding of the mechanistic processes that underpin the activation of different inflammasomes and their regulation —and dysregulation—by both host and pathogen will be covered.
Dr. James Harris
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 papers will be 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 monthly 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 1800 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.
The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.
Tentative Title: The roles of guanylate-binding proteins (GBPs) in activation of both canonical and noncanonical inflammasomes
Author: Anita Pinar
Tentative Title: Inflammasome activation during pathological fibrotic diseases
Author: Tae-Bong Kang
Tentative Title: The role of signal molecules of necroptosis in inflammasome activation
Abstract: Necroptotic cell death is believed to be associated with inflammation due to the release of cellular contents from damaged plasma membrane. However, growing evidences suggest that many of signal molecules known to regulate necroptotic death can also regulate inflammasome activation in a cell-intrinsic manner. Therefore, in this review, I will discuss about the current knowledge regarding the role of signal molecules of necroptosis in inflammasome activation.
Author: Ju-Young Moon
Tentative Title: The role of inflammasome-dependent and -independent NLRP3 in the kidney disease
Abstract: Many studies have investigated the activation of NLRP3 inflammasome in renal diseases, such as diabetic nephropathy, hypertensive kidney disease and rhabdomyolysis induced kidney injury. The regulation of NLRP3 genetically or pharmacologically, the progression of renal diseases was dampened. The NLRP3 inflammasome activated by various endogenous danger associated molecular patterns (DAMPs) in the kidney disease. Hyperuricemia without uric acid crystals acts as a DAMP activated NLRP3 inflammasome through mitochondrial ROS in the renal macrophages and secreted IL-1β affected to increase NF-κB expression in renal tubular cells. Recently, several evidences have shown NLRP3 could have a role in inflammasome-independent way in non-immune cells. Renal tubular cells have considerable amount of the NLRP3 protein but do not contain pro-IL-1β and secrete IL-1β. This review will outline the role of NLRP3 in the kidney disease and evaluate the NLRP3 as the potential therapeutic target.
Author: James Vince, Maryam Rashidi
Tentative Title: Mechanisms of particle-induced inflammasome activation and cell death