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Special Issue "New Molecular Mechanisms and Markers in Inflammatory Disorders"

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Biochemistry".

Deadline for manuscript submissions: 25 October 2022 | Viewed by 1106

Special Issue Editors

Prof. Dr. Galliera Emanuela Rita
E-Mail Website
Guest Editor
Department of Biomedical Sciences for Health, Università degli Studi di Milano, Milan, Italy
Interests: inflammation; inflammatory disorders; biomarkers; molecular mechanism of inflammation; molecular signaling
Prof. Dr. Elena Vianello
E-Mail Website
Guest Editor
Department of Biomedical Sciences for Health, Università degli Studi di Milano, Milan, Italy
Interests: inflammation; inflammatory disorders; biomarkers; molecular mechanism of inflammation; molecular signaling

Special Issue Information

Dear Colleagues,

Inflammation importantly participates in host defences against infectious agents and injury, but it also contributes to the pathophysiology of many chronic diseases, ranging from cancer to biomechanical injuries and from chronic to acute disorders. For this reason, the discovery of new inflammation-linked biomarkers is the goal of many studies focused on the pathogenesis, the diagnosis, the prognosis, and the therapeutical approaches of inflammatory-associated comorbidities. The intent of this Special Issue is to present research papers and reviews focused on the new biomarkers of inflammatory-associated disorders, which highlight the molecular mechanisms of inflammation in the onset and progression of pathological states like cancer, immune diseases, cardiovascular-associated disorders, metabolic diseases, and all other pathological states linked to inflammation. This knowledge should aid the development of novel strategies to predict disease susceptibility, target and monitor therapies, and ultimately develop new approaches to the prevention and treatment of diseases associated with inflammatory status.

Prof. Dr. Galliera Emanuela Rita
Prof. Dr. Elena Vianello
Guest Editors

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

  • inflammation
  • inflammatory disorders
  • biomarkers
  • molecular mechanism of inflammation
  • molecular signaling

Published Papers (2 papers)

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Research

Article
Regulation of Neuroinflammatory Signaling by PPARγ Agonist in Mouse Model of Diabetes
Int. J. Mol. Sci. 2022, 23(10), 5502; https://doi.org/10.3390/ijms23105502 - 14 May 2022
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Abstract
Many relevant studies, as well as clinical practice, confirm that untreated diabetes predisposes the development of neuroinflammation and cognitive impairment. Having regard for the fact that PPARγ are widely distributed in the brain and PPARγ ligands may regulate the inflammatory process, [...] Read more.
Many relevant studies, as well as clinical practice, confirm that untreated diabetes predisposes the development of neuroinflammation and cognitive impairment. Having regard for the fact that PPARγ are widely distributed in the brain and PPARγ ligands may regulate the inflammatory process, the anti-inflammatory potential of the PPARγ agonist, pioglitazone, was assessed in a mouse model of neuroinflammation related with diabetes. In this regard, the biochemical and molecular indicators of neuroinflammation were determined in the hippocampus and prefrontal cortex of diabetes mice. The levels of cytokines (IL-1β, IL-6, and TNF) and the expression of genes (Tnfrsf1a and Cav1) were measured. In addition, behavioral tests such as the open field test, the hole-board test, and the novel object recognition test were conducted. A 14-day treatment with pioglitazone significantly decreased IL-6 and TNFα levels in the prefrontal cortex and led to the downregulation of Tnfrsf1a expression and the upregulation of Cav1 expression in both brain regions of diabetic mice. Pioglitazone, by targeting neuroinflammatory signaling, improved memory and exploratory activity in behavioral tests. The present study provided a potential theoretical basis and therapeutic target for the treatment of neuroinflammation associated with diabetes. Pioglitazone may provide a promising therapeutic strategy in diabetes patients with muffled of behavioral activity. Full article
(This article belongs to the Special Issue New Molecular Mechanisms and Markers in Inflammatory Disorders)
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Article
A Wide-Proteome Analysis to Identify Molecular Pathways Involved in Kidney Response to High-Fat Diet in Mice
Int. J. Mol. Sci. 2022, 23(7), 3809; https://doi.org/10.3390/ijms23073809 - 30 Mar 2022
Viewed by 379
Abstract
The etiopathogenesis of obesity-related chronic kidney disease (CKD) is still scarcely understood. To this aim, we assessed the effect of high-fat diet (HF) on molecular pathways leading to organ damage, steatosis, and fibrosis. Six-week-old male C57BL/6N mice were fed HF diet or normal [...] Read more.
The etiopathogenesis of obesity-related chronic kidney disease (CKD) is still scarcely understood. To this aim, we assessed the effect of high-fat diet (HF) on molecular pathways leading to organ damage, steatosis, and fibrosis. Six-week-old male C57BL/6N mice were fed HF diet or normal chow for 20 weeks. Kidneys were collected for genomic, proteomic, histological studies, and lipid quantification. The main findings were as follows: (1) HF diet activated specific pathways leading to fibrosis and increased fatty acid metabolism; (2) HF diet promoted a metabolic shift of lipid metabolism from peroxisomes to mitochondria; (3) no signs of lipid accumulation and/or fibrosis were observed, histologically; (4) the early signs of kidney damage seemed to be related to changes in membrane protein expression; (5) the proto-oncogene MYC was one of the upstream transcriptional regulators of changes occurring in protein expression. These results demonstrated the potential usefulness of specific selected molecules as early markers of renal injury in HF, while histomorphological changes become visible later in obesity-related CDK. The integration of these information with data from biological fluids could help the identification of biomarkers useful for the early detection and prevention of tissue damage in clinical practice. Full article
(This article belongs to the Special Issue New Molecular Mechanisms and Markers in Inflammatory Disorders)
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