Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
9.0
6.0
Journals
Cells
Special Issues
Roles of Inflammasomes in Aging and Age-Related Diseases Ⅱ
share announcement

Roles of Inflammasomes in Aging and Age-Related Diseases Ⅱ

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Immunology".

Deadline for manuscript submissions: closed (1 October 2021) | Viewed by 12015

Special Issue Editor

Dr. Mario D. Cordero

E-Mail Website
Guest Editor
Instituto de Investigación e Innovación en Ciencias Biomédicas de Cádiz, INiBICA, 11009 Cádiz, Spain
Interests: inflammasomes; aging; autophagy; rare diseases
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear colleagues,

Inflammasomes are multiprotein complexes formed and activated after exposure to different danger signals that lead to the maturation of caspase-1 and the processing of its substrates, IL-1β and IL-18. In recent years, their implication in different diseases such as cardiovascular, neurodegenerative, psychiatric, and metabolic diseases has opened the door to developing new therapeutic perspectives. The NLRP3-inflammasome is the best-described complex which has also been shown to play a role in metabolic diseases such as obesity, diabetes, gout, and different age-associated diseases. Recently, the ablation of NLRP3 has been shown to prevent different aspects of aging and improve healthspan and lifespan in animal models.

In the Special Issue entitled “Inflammasomes in aging”, we welcome the submission of original and review articles covering a broad range of aspects related to the pathophysiological aspect of the inflammasomes in aging and age-related diseases. This may include topics related to cancer, cardiovascular, metabolic, neurodegenerative, and psychiatric diseases, bone disorder, and all disorder associated with aging. Furthermore, we may include biological topics associated with inflammasomes and aging; autophagy; AMPK; inflammation; stem cells; immunology; pathogens; oxidative stress; mitochondrial dysfunction; and cellular stress.

Dr. Mario D. Cordero
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

  • inflammasomes
  • NLRP3
  • aging
  • age-related diseases

Published Papers (3 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

Jump to: Review

14 pages, 2135 KiB  
Article
Regulation of Inflammasomes by Application of Omega-3 Polyunsaturated Fatty Acids in a Spinal Cord Injury Model
by Maryam Baazm, Victoria Behrens, Cordian Beyer, Omid Nikoubashman and Adib Zendedel
Cells 2021, 10(11), 3147; https://doi.org/10.3390/cells10113147 - 12 Nov 2021
Cited by 11 | Viewed by 2017
Abstract
Omega-3 polyunsaturated fatty acids (PUFA n3) ameliorate inflammation in different diseases and potentially improve neurological function after neuronal injury. Following spinal cord injury (SCI), inflammatory events result in caspase-1 mediated activation of interleukin-1 beta (IL-1b) and 18. We aim to evaluate the neuroprotective [...] Read more.
Omega-3 polyunsaturated fatty acids (PUFA n3) ameliorate inflammation in different diseases and potentially improve neurological function after neuronal injury. Following spinal cord injury (SCI), inflammatory events result in caspase-1 mediated activation of interleukin-1 beta (IL-1b) and 18. We aim to evaluate the neuroprotective potency of PUFA n3 in suppressing the formation and activation of inflammasomes following SCI. Male Wistar rats were divided into four groups: control, SCI, SCI+PUFA n3, and SCI+Lipofundin MCT (medium-chain triglyceride; vehicle). PUFA n3 or vehicle was intravenously administered immediately after SCI and every 24 h for the next three days. We analyzed the expression of NLRP3, NLRP1, ASC, caspase-1, IL-1b, and 18 in the spinal cord. The distribution of microglia, oligodendrocytes, and astrocytes was assessed by immunohistochemistry analysis. Behavioral testing showed significantly improved locomotor recovery in PUFA n3-treated animals and the SCI-induced upregulation of inflammasome components was reduced. Histopathological evaluation confirmed the suppression of microgliosis, increased numbers of oligodendrocytes, and the prevention of demyelination by PUFA n3. Our data support the neuroprotective role of PUFA n3 by targeting the NLRP3 inflammasome. These findings provide evidence that PUFA n3 has therapeutic effects which potentially attenuate neuronal damage in SCI and possibly also in other neuronal injuries. Full article
(This article belongs to the Special Issue Roles of Inflammasomes in Aging and Age-Related Diseases Ⅱ)
►▼ Show Figures

Figure 1

10 pages, 2512 KiB  
Article
Lower Temperatures Exacerbate NLRP3 Inflammasome Activation by Promoting Monosodium Urate Crystallization, Causing Gout
by Huijeong Ahn, Gilyoung Lee and Geun-Shik Lee
Cells 2021, 10(8), 1919; https://doi.org/10.3390/cells10081919 - 29 Jul 2021
Cited by 13 | Viewed by 2194
Abstract
Gout is a recurrent and chronic form of arthritis caused by the deposition of monosodium urate (MSU) crystals in the joints. Macrophages intake MSU crystals, the trigger for NLRP3 inflammasome activation, which leads to the release of interleukin (IL)-1β and results in the [...] Read more.
Gout is a recurrent and chronic form of arthritis caused by the deposition of monosodium urate (MSU) crystals in the joints. Macrophages intake MSU crystals, the trigger for NLRP3 inflammasome activation, which leads to the release of interleukin (IL)-1β and results in the flaring of gout. The effects of temperature, an environmental factor for MSU crystallization, on IL-1β secretion have not been well studied. This study examined the effects of temperature on inflammasome activation. Specific triggers activated canonical inflammasomes (NLRP3, NLRC4, and AIM2) in murine macrophages at various temperatures (25, 33, 37, 39, and 42 °C). The maturation of IL-1β and caspase-1 was measured as an indicator for inflammasome activation. As expected, the optimal temperature of inflammasome activation was 37 °C. The MSU crystal-mediated activation of inflammasome increased at temperatures lower than 37 °C and decreased at higher temperatures. MSU crystals at lower temperatures enhanced IL-1β secretion via the NLRP3 inflammasome pathway. A lower temperature promoted the formation of MSU crystals without changing phagocytosis. Overall, lower temperatures form more MSU crystals and enhance NLRP3 inflammasome activation. In light of these findings, it is possible that hyperthermia therapy may reduce gout flaring. Full article
(This article belongs to the Special Issue Roles of Inflammasomes in Aging and Age-Related Diseases Ⅱ)
►▼ Show Figures

Figure 1

Review

Jump to: Research

21 pages, 2399 KiB  
Review
Inflammasomes in the Pathophysiology of Aortic Disease
by Markus Wortmann, Andreas S. Peters, Philipp Erhart, Daniel Körfer, Dittmar Böckler and Susanne Dihlmann
Cells 2021, 10(9), 2433; https://doi.org/10.3390/cells10092433 - 15 Sep 2021
Cited by 28 | Viewed by 7275
Abstract
Aortic diseases comprise aneurysms, dissections, and several other pathologies. In general, aging is associated with a slow but progressive dilation of the aorta, along with increased stiffness and pulse pressure. The progression of aortic disease is characterized by subclinical development or acute presentation. [...] Read more.
Aortic diseases comprise aneurysms, dissections, and several other pathologies. In general, aging is associated with a slow but progressive dilation of the aorta, along with increased stiffness and pulse pressure. The progression of aortic disease is characterized by subclinical development or acute presentation. Recent evidence suggests that inflammation participates causally in different clinical manifestations of aortic diseases. As of yet, diagnostic imaging and surveillance is mainly based on ultrasonography, computed tomography (CT), and magnetic resonance imaging (MRI). Little medical therapy is available so far to prevent or treat the majority of aortic diseases. Endovascular therapy by the introduction of covered stentgrafts provides the main treatment option, although open surgery and implantation of synthetic grafts remain necessary in many situations. Because of the risks associated with surgery, there is a need for identification of pharmaceutical targets interfering with the pathophysiology of aortic remodeling. The participation of innate immunity and inflammasome activation in different cell types is common in aortic diseases. This review will thus focus on inflammasome activities in vascular cells of different chronic and acute aortic diseases and discuss their role in development and progression. We will also identify research gaps and suggest promising therapeutic targets, which may be used for future medical interventions. Full article
(This article belongs to the Special Issue Roles of Inflammasomes in Aging and Age-Related Diseases Ⅱ)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-3
Back to TopTop