Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
5.7
3.6
Journals
Biology
Special Issues
Biochemical Evaluation of Altered Signaling Pathways in Pathophysiological Conditions Associated...
share announcement

Biochemical Evaluation of Altered Signaling Pathways in Pathophysiological Conditions Associated with Inflammatory Disorders

A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Biochemistry and Molecular Biology".

Deadline for manuscript submissions: closed (15 August 2021) | Viewed by 35870

Special Issue Editors

Dr. Roberta Fusco

E-Mail Website
Guest Editor
Department of Chemical, Biological, Pharmaceutical and Environmental Sciences, University of Messina, 98166 Messina, Italy
Interests: biochemistry; diet; mithocondrial disfunction; oxidative stress; molecular pathways
Special Issues, Collections and Topics in MDPI journals
Dr. Ramona D'Amico

E-Mail Website
Co-Guest Editor
Department of Chemical Biological, Pharmaceutical and Environmental Sciences, Università degli Studi di Messina, 98166 Messina, Italy
Interests: biomarkers; molecular pathways; oxidative stress; inflammation; natural compound; clinical and pre-clinical studies
Special Issues, Collections and Topics in MDPI journals
Dr. Alesso Filippo Peritore

E-Mail Website
Co-Guest Editor
Department of Chemical, Biological, Pharmaceutical and Environmental Science, University of Messina, 98166 Messina, Italy
Interests: environmental pollutants; ecotoxicology; inflammation; marine biotechnology; biochemistry
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Oxidative stress, such as that due to free radicals and/or reactive oxygen species, is known to cause organ injury. A growing body of evidence indicates that oxidative stress plays an important role in the pathogenesis of inflammatory diseases, including cardiovascular diseases, liver diseases, lung disease, gastrointestinal disorders, neurological disorders, muscle damage, and diabetes, as well as in aging. The imbalance between the production of oxidants and their elimination damages cells and tissues, triggering necrosis or apoptosis, amplifying the pro-inflammatory response, and destroying histological organization. The endothelial dysfunction produced by the injury leads to the recruitmnet of polymorphonuclear leukocytes to the lesion site, involving a complex system of adhesion molecules. Neutrophil activation, in turn, induces a large production of superoxide anions (O2•−), lipid peroxidation and oxidation, and DNA single-strand damage. The nuclear factor E2-related factor 2 (Nrf2) pathway is described to have a critical role in oxidative stress. It and its target genes are considered multiple-organ protectors thanks to their cyto-protective and anti-oxidative functions. On the basis of the free radical theory, numerous studies examined the effects of antioxidant supplementation therapies in seveal inflammatory pathologies.

This Special Issue will focus on both in vitro and in vivo studies investigating the effect of natural (antioxidant-rich foods) and synthetic antioxidant molecules on inflammatory pathologies in humans, pets, and farm animals. Moreover, this Special Issue will welcome reviews and original studies providing evidence of the effect of antioxidant factors on acute and cronic diseases.

Dr. Roberta Fusco
Guest Editor
Dr. Ramona D'Amico
Dr. Alessio Peritore
Co-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. Biology 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 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

  • oxidative stress 
  • inflammation 
  • biochemical markers 
  • enzyme activity 
  • physiological alteration 
  • phytochemicals 
  • Nrf2

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • e-Book format: Special Issues with more than 10 articles can be published as dedicated e-books, ensuring wide and rapid dissemination.

Further information on MDPI's Special Issue polices can be found here.

Published Papers (4 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

15 pages, 1100 KiB  
Article
The Effect of Intensive Dietary Intervention on the Level of RANTES and CXCL4 Chemokines in Patients with Non-Obstructive Coronary Artery Disease: A Randomised Study
by Magdalena Makarewicz-Wujec, Jan Henzel, Mariusz Kruk, Cezary Kępka, Łukasz Wardziak, Piotr Trochimiuk, Andrzej Parzonko, Marcin Demkow, Zofia Dzielińska and Malgorzata Kozłowska-Wojciechowska
Biology 2021, 10(2), 156; https://doi.org/10.3390/biology10020156 - 16 Feb 2021
Cited by 3 | Viewed by 2359
Abstract
Background: Inflammation is the key pathophysiological mechanism of the initiation and progression of atherosclerosis. The study objective was to assess the effects of a dietary intervention based on the model of the dietary approaches to stop hypertension (DASH) diet on the levels of [...] Read more.
Background: Inflammation is the key pathophysiological mechanism of the initiation and progression of atherosclerosis. The study objective was to assess the effects of a dietary intervention based on the model of the dietary approaches to stop hypertension (DASH) diet on the levels of chemokines RANTES and CXCL4 in patients with non-obstructive coronary artery disease. Methods: As part of Dietary Intervention to Stop Coronary Atherosclerosis in Computed Tomography (DISCO-CT) study, patients were randomised to an intervention group (n = 40), where the DASH diet was introduced along with optimal pharmacotherapy, and to a control group (n = 39), with optimal pharmacotherapy alone. In the DASH group, systematic dietary counselling was provided for the follow-up period. RANTES and CXCL4 levels were determined using ELISA. Results: In the DASH group, the RANTES level insignificantly reduced from 42.70 ± 21.1 ng/mL to 38.09 ± 18.5 ng/mL (p = 0.134), and the CXCL4 concentration significantly reduced from 12.38 ± 4.1 ng/mL to 8.36 ± 2.3 ng/mL (p = 0.0001). At the same time, an increase in the level of both chemokines was observed in the control group: RANTES from 34.69 ± 22.7 to 40.94 ± 20.0 ng/mL (p = 0.06) and CXCL4 from 10.98 ± 3.6 to 13.0 5± 4.8 ng/mL (p = 0.009). The difference between the changes in both groups was significant for both RANTES (p = 0.03) and CXCL4 (p = 0.00001). The RANTES/CXCL4 ratio reduced in the control group (from 3.52 ± 2.8 to 3.35 ± 2.8; p = 0.006), while in the DASH group, an increase was observed (from 3.54 ± 1.7 to 4.77 ± 2.4; p = 0.001). Conclusions: A 12-month-long intensive dietary intervention based on DASH diet guidelines as an addition to optimal pharmacotherapy causes changes in the levels of chemokines CXCL4 and RANTES and their mutual relationship in comparison to conventional treatment. Full article
(This article belongs to the Special Issue Biochemical Evaluation of Altered Signaling Pathways in Pathophysiological Conditions Associated with Inflammatory Disorders)
►▼ Show Figures

Figure 1

14 pages, 16258 KiB  
Article
Long-Term Aspartame Administration Leads to Fibrosis, Inflammasome Activation, and Gluconeogenesis Impairment in the Liver of Mice
by Isabela A. Finamor, Caroline A. Bressan, Isabel Torres-Cuevas, Sergio Rius-Pérez, Marcelo da Veiga, Maria I. Rocha, Maria A. Pavanato and Salvador Pérez
Biology 2021, 10(2), 82; https://doi.org/10.3390/biology10020082 - 22 Jan 2021
Cited by 17 | Viewed by 15714
Abstract
Background: Aspartame is an artificial sweetener used in foods and beverages worldwide. However, it is linked to oxidative stress, inflammation, and liver damage through mechanisms that are not fully elucidated yet. This work aimed to investigate the effects of long-term administration of aspartame [...] Read more.
Background: Aspartame is an artificial sweetener used in foods and beverages worldwide. However, it is linked to oxidative stress, inflammation, and liver damage through mechanisms that are not fully elucidated yet. This work aimed to investigate the effects of long-term administration of aspartame on the oxidative and inflammatory mechanisms associated with liver fibrosis progression in mice. Methods: Mice were divided into two groups with six animals each: control and aspartame. Aspartame (80 mg/kg, via oral) or vehicle was administrated for 12 weeks. Results: Aspartame caused liver damage and elevated serum transaminase levels. Aspartame also generated liver fibrosis, as evidenced by histology analysis, and pro-fibrotic markers’ upregulation, including transforming growth factor β 1, collagen type I alpha 1, and alpha-smooth muscle actin. Furthermore, aspartame reduced nuclear factor erythroid 2-related factor 2 (Nrf2) activation and enzymatic antioxidant activity and increased lipid peroxidation, which triggered NOD-like receptor containing protein 3 (NLRP3) inflammasome activation and p53 induction. Furthermore, aspartame reduced peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC-1α) levels, possibly through p53 activation. This PGC-1α deficiency could be responsible for the changes in lipid profile in serum, total lipid accumulation, and gluconeogenesis impairment in liver, evidenced by the gluconeogenic enzymes’ downregulation, thus causing hypoglycemia. Conclusions: This work provides new insights to understand the mechanisms related to the adverse effects of aspartame on liver tissue. Full article
(This article belongs to the Special Issue Biochemical Evaluation of Altered Signaling Pathways in Pathophysiological Conditions Associated with Inflammatory Disorders)
►▼ Show Figures

Graphical abstract

30 pages, 10724 KiB  
Article
Formyl Peptide Receptor 1 Signaling in Acute Inflammation and Neural Differentiation Induced by Traumatic Brain Injury
by Roberta Fusco, Enrico Gugliandolo, Rosalba Siracusa, Maria Scuto, Marika Cordaro, Ramona D’Amico, Maurizio Evangelista, Angelo Peli, Alessio Filippo Peritore, Daniela Impellizzeri, Rosalia Crupi, Salvatore Cuzzocrea and Rosanna Di Paola
Biology 2020, 9(9), 238; https://doi.org/10.3390/biology9090238 - 20 Aug 2020
Cited by 61 | Viewed by 4778
Abstract
Traumatic brain injury (TBI) is a shocking disease frequently followed by behavioral disabilities, including risk of cerebral atrophy and dementia. N-formylpeptide receptor 1 (FPR1) is expressed in cells and neurons in the central nervous system. It is involved in inflammatory processes and during [...] Read more.
Traumatic brain injury (TBI) is a shocking disease frequently followed by behavioral disabilities, including risk of cerebral atrophy and dementia. N-formylpeptide receptor 1 (FPR1) is expressed in cells and neurons in the central nervous system. It is involved in inflammatory processes and during the differentiation process in the neural stem cells. We investigate the effect of the absence of Fpr1 gene expression in mice subjected to TBI from the early stage of acute inflammation to neurogenesis and systematic behavioral testing four weeks after injury. C57BL/6 animals and Fpr1 KO mice were subjected to TBI and sacrificed 24 h or four weeks after injury. Twenty-four hours after injury, TBI Fpr1 KO mice showed reduced histological impairment, tissue damage and acute inflammation (MAPK activation, NF-κB signaling induction, NRLP3 inflammasome pathway activation and oxidative stress increase). Conversely, four weeks after TBI, the Fpr1 KO mice showed reduced survival of the proliferated cells in the Dentate Gyrus compared to the WT group. Behavioral analysis confirmed this trend. Moreover, TBI Fpr1 KO animals displayed reduced neural differentiation (evaluated by beta-III tubulin expression) and upregulation of astrocyte differentiation (evaluated by GFAP expression). Collectively, our study reports that, immediately after TBI, Fpr1 increased acute inflammation, while after four weeks, Fpr1 promoted neurogenesis. Full article
(This article belongs to the Special Issue Biochemical Evaluation of Altered Signaling Pathways in Pathophysiological Conditions Associated with Inflammatory Disorders)
►▼ Show Figures

Graphical abstract

Review

Jump to: Research

29 pages, 1390 KiB  
Review
Telomere Length and Oxidative Stress and Its Relation with Metabolic Syndrome Components in the Aging
by Graciela Gavia-García, Juana Rosado-Pérez, Taide Laurita Arista-Ugalde, Itzen Aguiñiga-Sánchez, Edelmiro Santiago-Osorio and Víctor Manuel Mendoza-Núñez
Biology 2021, 10(4), 253; https://doi.org/10.3390/biology10040253 - 24 Mar 2021
Cited by 66 | Viewed by 12043
Abstract
A great amount of scientific evidence supports that Oxidative Stress (OxS) can contribute to telomeric attrition and also plays an important role in the development of certain age-related diseases, among them the metabolic syndrome (MetS), which is characterised by clinical and biochemical alterations [...] Read more.
A great amount of scientific evidence supports that Oxidative Stress (OxS) can contribute to telomeric attrition and also plays an important role in the development of certain age-related diseases, among them the metabolic syndrome (MetS), which is characterised by clinical and biochemical alterations such as obesity, dyslipidaemia, arterial hypertension, hyperglycaemia, and insulin resistance, all of which are considered as risk factors for type 2 diabetes mellitus (T2DM) and cardiovascular diseases, which are associated in turn with an increase of OxS. In this sense, we review scientific evidence that supports the association between OxS with telomere length (TL) dynamics and the relationship with MetS components in aging. It was analysed whether each MetS component affects the telomere length separately or if they all affect it together. Likewise, this review provides a summary of the structure and function of telomeres and telomerase, the mechanisms of telomeric DNA repair, how telomere length may influence the fate of cells or be linked to inflammation and the development of age-related diseases, and finally, how the lifestyles can affect telomere length. Full article
(This article belongs to the Special Issue Biochemical Evaluation of Altered Signaling Pathways in Pathophysiological Conditions Associated with Inflammatory Disorders)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-4
Back to TopTop