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Immune-Inflammatory and Oxidative Stress Signaling Pathways Involved in Human Disorders

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

Deadline for manuscript submissions: closed (28 April 2024) | Viewed by 1848

Special Issue Editors


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Guest Editor
Department of Chemical, Biological, Pharmaceutical and Environmental Sciences, University of Messina, Viale Ferdinando Stagno D’Alcontres, 31, 98166 Messina, Italy
Interests: inflammation; oxidative stress; cancer; animal model; meta-analysis

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Guest Editor
Department of Chemical, Biological, Pharmaceutical and Environmental Sciences, University of Messina, 98122 Messina, Italy
Interests: neuroinflammation; neuromodulation; astrocytes; spinal cord injury; brain trauma; cytokines; neurodegenerative disorders; brain tumors
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Special Issue Information

Dear Colleagues,

Inflammation is a physiological process that occurs in response to the presence of a foreign organism, including human pathogens, dust particles, and viruses. If not adequately controlled, inflammation, in its acute or chronic states, can trigger a series of biological processes that, cooperatively with the impaired immune response and oxidative stress, affect the physiological cellular mechanisms, disadvantaging cellular homeostasis in various body areas. Therefore, this Special Issue aims to cover the current state of the art of preclinical studies and clinical studies combined with molecular data, including original research articles, full reviews, systematic reviews and meta-analyses evaluating molecular pathways involved in immune-inflammation and oxidative stress that represent a common denominator of various human pathologies. The modulation of these molecular pathways using synthetic or natural compounds and the discovery of new pathogenic biomarkers represent important goals for scientific research in the management of various pathologies such as neurodegenerative diseases, neurotraumas, cardiovascular, oncology and immune-related pathologies (IBD, skin diseases or genetics).

Dr. Alessio Ardizzone
Prof. Dr. Emanuela Esposito
Guest Editors

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Keywords

  • inflammation
  • neuroinflammation
  • immune system
  • oxidative stress

Published Papers (2 papers)

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Research

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19 pages, 4097 KiB  
Article
Novel Findings on CCR1 Receptor in CNS Disorders: A Pathogenic Marker Useful in Controlling Neuroimmune and Neuroinflammatory Mechanisms in Parkinson’s Disease
by Alberto Repici, Anna Paola Capra, Ahmed Hasan, Maria Bulzomì, Michela Campolo, Irene Paterniti, Emanuela Esposito and Alessio Ardizzone
Int. J. Mol. Sci. 2024, 25(8), 4337; https://doi.org/10.3390/ijms25084337 - 14 Apr 2024
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Abstract
Parkinson’s disease (PD) is recognized as the second most common neurodegenerative disease worldwide. Even if PD etiopathogenesis is not yet fully understood, in recent years, it has been advanced that a chronic state of inflammation could play a decisive role in the development [...] Read more.
Parkinson’s disease (PD) is recognized as the second most common neurodegenerative disease worldwide. Even if PD etiopathogenesis is not yet fully understood, in recent years, it has been advanced that a chronic state of inflammation could play a decisive role in the development of this pathology, establishing the close link between PD and neuroinflammation. In the broad panorama of inflammation and its several signaling pathways, the C-C chemokine receptor type 1 (CCR1) could play a key pathogenic role in PD progression, and could constitute a valuable target for the development of innovative anti-PD therapies. In this study, we probed the neuroprotective properties of the CCR1 antagonist BX471 compound in a mouse model of MPTP-induced nigrostriatal degeneration. BX471 treatments were performed intraperitoneally at a dose of 3 mg/kg, 10 mg/kg, and 30 mg/kg, starting 24 h after the last injection of MPTP and continuing for 7 days. From our data, BX471 treatment strongly blocked CCR1 and, as a result, decreased PD features, also reducing the neuroinflammatory state by regulating glial activation, NF-κB pathway, proinflammatory enzymes, and cytokines overexpression. Moreover, we showed that BX471’s antagonistic action on CCR1 reduced the infiltration of immune cells, including mast cells and lymphocyte T activation. In addition, biochemical analyses carried out on serum revealed a considerable increase in circulating levels of CCR1 following MPTP-induced PD. In light of these findings, CCR1 could represent a useful pathological marker of PD, and its targeting could be a worthy candidate for the future development of new immunotherapies against PD. Full article
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17 pages, 1254 KiB  
Review
Highlights on the Effects of Non-Coding RNAs in the Osteonecrosis of the Jaw
by Santino Caserta, Fabio Stagno, Sebastiano Gangemi and Alessandro Allegra
Int. J. Mol. Sci. 2024, 25(3), 1598; https://doi.org/10.3390/ijms25031598 - 27 Jan 2024
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Abstract
Osteonecrosis of the jaw is the progressive loss and destruction of bone affecting the maxilla or mandible in patients treated with antiresorptive and antiangiogenic agents without receiving prior radiation therapy. The pathogenesis involves the inflammatory pathway of receptor activator of nuclear factor NF-kB [...] Read more.
Osteonecrosis of the jaw is the progressive loss and destruction of bone affecting the maxilla or mandible in patients treated with antiresorptive and antiangiogenic agents without receiving prior radiation therapy. The pathogenesis involves the inflammatory pathway of receptor activator of nuclear factor NF-kB ligand and the macrophage colony-stimulating factor, essential for osteoclast precursors survival and proliferation and acting through its receptor c-Fms. Evidence has shown the role of non-coding RNAs in the pathogenesis of osteonecrosis of the jaw and this finding might be useful in diagnosis since these small RNAs could be considered as biomarkers of apoptotic activity in bone. Interestingly, it has been proved that miR-29 and miR-31-5p, acting on specific targets such as CALCR and RhoA, promote programmed-cell death and consequently the necrosis of bone tissue. Specific long non-coding RNAs, instead, have been detected both at reduced levels in patients with multiple myeloma and osteonecrosis, and associated with suppression of osteoblast differentiation, with consequences in the progression of mandible lesions. Among non-coding genic material, circular RNAs have the capability to modify the expression of specific mRNAs responsible for the inhibition of bisphosphonates activity on osteoclastogenesis. Full article
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