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IJMS
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Sepsis: From Molecular Mechanisms, Pathophysiology to Novel Therapeutic Approaches 4.0
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Sepsis: From Molecular Mechanisms, Pathophysiology to Novel Therapeutic Approaches 4.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 30 May 2024 | Viewed by 1397

Special Issue Editor

Prof. Dr. Andreas Von Knethen

E-Mail Website
Guest Editor
Institute of Biochemistry I, Faculty of Medicine, Goethe-University, Frankfurt am Main, Germany
Interests: sepsis; Nrf2; PPARγ; redox signaling; autophagy
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

It is our pleasure to announce the launch of the Special Issue of IJMS, entitled “Sepsis: From Molecular Mechanisms, Pathophysiology to Novel Therapeutic Approaches 4.0”. Considering that antibiosis, the eradication of the focus, and intensive care supply are the only treatment regimens suitable for patients suffering from sepsis, it is obvious that new therapies are required. Because the anamneses of patients are very heterogeneous, characterizing mechanistic details associated with sepsis initiation or progression will be helpful to setting up new therapeutic approaches. Therefore, we welcome manuscripts elucidating molecular mechanisms in vitro or in vivo in preclinical models as well as studies from patients providing insights into new therapeutic concepts to prevent or treat sepsis progression. Based on this research topic, we plan to publish a combination of original research manuscripts and review articles in the field of the origin of sepsis and deviated therapies.

Review and original articles that cover, but are not limited to, the following topics are welcome:

  • Cell culture studies, characterizing and/or identifying new factors involved in sepsis development;
  • The role of immune cell subpopulations in sepsis progression;
  • Animal models providing mechanistic insights of underlying principles leading to sepsis;
  • Therapeutic approaches to prevent or cure sepsis and future perspectives;
  • Definition of new sepsis biomarkers;
  • Characterization of putative subgroups of sepsis patients with a similar origin of sepsis.

Prof. Dr. Andreas Von Knethen
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • sepsis
  • animal models
  • therapy concept
  • biomarkers
  • immune suppression
  • epigenetics

Published Papers (2 papers)

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Research

12 pages, 880 KiB  
Article
The Association between the rs3747406 Polymorphism in the Glucocorticoid-Induced Leucine Zipper Gene and Sepsis Survivals Depends on the SOFA Score
by Stefan Rusev, Patrick Thon, Tim Rahmel, Dominik Ziehe, Britta Marko, Hartmuth Nowak, Björn Ellger, Ulrich Limper, Elke Schwier, Dietrich Henzler, Stefan Felix Ehrentraut, Lars Bergmann, Matthias Unterberg, Michael Adamzik, Björn Koos, Katharina Rump and SepsisDataNet.NRW Research Group
Int. J. Mol. Sci. 2024, 25(7), 3871; https://doi.org/10.3390/ijms25073871 - 30 Mar 2024
Viewed by 515
Abstract
The variability in mortality in sepsis could be a consequence of genetic variability. The glucocorticoid system and the intermediate TSC22D3 gene product—glucocorticoid-induced leucine zipper—are clinically relevant in sepsis, which is why this study aimed to clarify whether TSC22D3 gene polymorphisms contribute to the [...] Read more.
The variability in mortality in sepsis could be a consequence of genetic variability. The glucocorticoid system and the intermediate TSC22D3 gene product—glucocorticoid-induced leucine zipper—are clinically relevant in sepsis, which is why this study aimed to clarify whether TSC22D3 gene polymorphisms contribute to the variance in sepsis mortality. Blood samples for DNA extraction were obtained from 455 patients with a sepsis diagnosis according to the Sepsis-III criteria and from 73 control subjects. A SNP TaqMan assay was used to detect single-nucleotide polymorphisms (SNPs) in the TSC22D3 gene. Statistical and graphical analyses were performed using the SPSS Statistics and GraphPad Prism software. C-allele carriers of rs3747406 have a 2.07-fold higher mortality rate when the sequential organ failure assessment (SOFA) score is higher than eight. In a multivariate COX regression model, the SNP rs3747406 with a SOFA score ≥ 8 was found to be an independent risk factor for 30-day survival in sepsis. The HR was calculated to be 2.12, with a p-value of 0.011. The wild-type allele was present in four out of six SNPs in our cohort. The promoter of TSC22D3 was found to be highly conserved. However, we discovered that the C-allele of rs3747406 poses a risk for sepsis mortality for SOFA Scores higher than 6. Full article
(This article belongs to the Special Issue Sepsis: From Molecular Mechanisms, Pathophysiology to Novel Therapeutic Approaches 4.0)
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11 pages, 3467 KiB  
Article
Oxidative Stress in Sepsis: A Focus on Cardiac Pathology
by Giuseppe Bertozzi, Michela Ferrara, Aldo Di Fazio, Aniello Maiese, Giuseppe Delogu, Nicola Di Fazio, Vittoria Tortorella, Raffaele La Russa and Vittorio Fineschi
Int. J. Mol. Sci. 2024, 25(5), 2912; https://doi.org/10.3390/ijms25052912 - 02 Mar 2024
Cited by 1 | Viewed by 571
Abstract
This study aims to analyze post-mortem human cardiac specimens, to verify and evaluate the existence or extent of oxidative stress in subjects whose cause of death has been traced to sepsis, through immunohistological oxidative/nitrosative stress markers. Indeed, in the present study, i-NOS, NOX2, [...] Read more.
This study aims to analyze post-mortem human cardiac specimens, to verify and evaluate the existence or extent of oxidative stress in subjects whose cause of death has been traced to sepsis, through immunohistological oxidative/nitrosative stress markers. Indeed, in the present study, i-NOS, NOX2, and nitrotyrosine markers were higher expressed in the septic death group when compared to the control group, associated with also a significant increase in 8-OHdG, highlighting the pivotal role of oxidative stress in septic etiopathogenesis. In particular, 70% of cardiomyocyte nuclei from septic death specimens showed positivity for 8-OHdG. Furthermore, intense and massive NOX2-positive myocyte immunoreaction was noticed in the septic group, as nitrotyrosine immunostaining intense reaction was found in the cardiac cells. These results demonstrated a correlation between oxidative and nitrosative stress imbalance and the pathophysiology of cardiac dysfunction documented in cases of sepsis. Therefore, subsequent studies will focus on the expression of oxidative stress markers in other organs and tissues, as well as on the involvement of the intracellular pattern of apoptosis, to better clarify the complex pathogenesis of multi-organ failure, leading to support the rationale for including therapies targeting redox abnormalities in the management of septic patients. Full article
(This article belongs to the Special Issue Sepsis: From Molecular Mechanisms, Pathophysiology to Novel Therapeutic Approaches 4.0)
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