Recent Advances in Metabolism and Oxidative Stress in Human Diseases 2.0

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

Deadline for manuscript submissions: 31 May 2025 | Viewed by 3047

Special Issue Editors


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Guest Editor
Dip.to di Farmacia (DIFAR), Scuola di Scienze Mediche e Farmaceutiche, Università degli Studi di Genova, V.le Benedetto XV, 3, 16132 Genoa, Italy
Interests: bioenergetics; neurosciences; metabolism; photoreceptor
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Guest Editor
Assistant Professor, Department of Experimental Medicine, University of Genoa, Genoa, Italy
Interests: bioenergetics; metabolism; redox status; antioxidant responses

Special Issue Information

Dear Colleagues,

Cell energy metabolism, the biochemical process responsible for ATP synthesis linked to NAD(P)H turnover, implies the occurrence of oxidative and reductive processes for metabolic energy recruitment and management. Most cell ATP is produced via mitochondrial oxidative phosphorylation (OxPhos), whose efficacy depends on mitochondria networks and ER–mitochondria interactions.

Recent studies have shown that the impairment of structural and functional interactions between ER and mitochondria, in addition to the  alteration of the mitochondrial network, affects cell physiology, resulting in the hyperproduction of reactive oxygen species (ROS) and oxidative damage. Although mitochondria represent the center of energy production, they also constitute the principal intracellular sources of ROS. This “double-edged role” configures mitochondria as the organelles in which the energy metabolism encounters redox homeostasis. Indeed, energy metabolism and redox state are inextricably linked in the coordinated regulation of (i) metabolic pathways, (ii) antioxidant systems, (iii) mitochondrial biogenesis and dynamics, and (iv) autophagy and mitophagy. Alterations of the crosstalk between redox homeostasis and cellular metabolism are hallmarks of a wide variety of disease processes. For example, in neurodegenerative disorders like Alzheimer’s and Parkinson’s diseases, oxidative stress has been identified as a key player associated with defects in mitochondrial function, dynamics, and/or degradation. Cardiovascular diseases also exhibit a strong connection with oxidative stress and mitochondrial dysregulation. Metabolic reprogramming of most core metabolic pathways, including those of glucose, glutamine, amino acids, and lipids, as well as increased antioxidant activity, are hallmarks of cancer cells in the various stages of the disease. Moreover, the tumor microenvironment (TME) represents a determinant metabolic barrier that affects T-cell anti-tumor activity. Indeed, the metabolic and nutrient competition in TME implies a metabolic reprogramming of T cells, rendering them dysfunctional and configuring this metabolic switch as a target in order to enhance T-cell-mediated immunity against cancer cells. Notably, recent evidence highlights the connection between ER stress response, oxidative stress, and inflammation in various diseases, emphasizing their roles in immunity and inflammatory/metabolic functions. Understanding the mechanisms and actors involved in the intricate crosstalk between energy metabolism and redox state has the potential to help to identify new therapeutic targets. 

This Special Issue, entitled “Recent Advances in Metabolism and Oxidative Stress in Human Diseases 2.0”, invites original research and review articles to contribute to the understanding of the molecular mechanisms that drive metabolic reprogramming, including the metabolic function, biology and redox homeostasis that lead to the development of effective treatments for different diseases.

Prof. Dr. Isabella Panfoli
Dr. Vanessa Cossu
Guest Editors

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Keywords

  • antioxidant responses
  • redox balance
  • ROS
  • hematologic oncology
  • solid tumors
  • immune response
  • ATP
  • cancer cells
  • mitochondria-ER interactions
  • endoplasmic reticulum
  • glucose metabolism
  • inflammation
  • mitochondria
  • mitochondrial dynamics
  • autophagy
  • mitophagy
  • metabolic plasticity
  • metabolism

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Related Special Issue

Published Papers (2 papers)

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Research

14 pages, 2069 KiB  
Article
Role of Oxidative Stress and Inflammation in Postoperative Complications and Quality of Life After Laryngeal Cancer Surgery
by Andjela Zivkovic, Ana Jotic, Ivan Dozic, Simona Randjelovic, Ivana Cirkovic, Branislava Medic, Jovica Milovanovic, Aleksandar Trivić, Aleksa Korugic, Ivan Vukasinović and Katarina Savic Vujovic
Cells 2024, 13(23), 1951; https://doi.org/10.3390/cells13231951 - 23 Nov 2024
Viewed by 959
Abstract
(1) Background: Laryngeal surgery due to carcinoma leads to significant tissue disruption, cellular injury, and inflammation. This leads to increased levels of reactive oxygen species (ROS), causing oxidative damage that can influence quality of life (QOL) and recovery and complicate the postoperative course. [...] Read more.
(1) Background: Laryngeal surgery due to carcinoma leads to significant tissue disruption, cellular injury, and inflammation. This leads to increased levels of reactive oxygen species (ROS), causing oxidative damage that can influence quality of life (QOL) and recovery and complicate the postoperative course. The aim of this study was to compare how postoperative quality of life and surgical complication occurrence interacted with the biomarker levels of oxidative stress (malondialdehyde, MDA; superoxide dismutase, SOD; glutathione peroxidase 1, GPX1; and catalase, CAT) and inflammation (interleukin 1, IL-1; interleukin 6, IL-6; C-reactive protein, CRP) in patients treated with conservative and radical laryngeal surgery. (2) Methods: The study included 56 patients who underwent surgical treatment for laryngeal cancer. Blood samples were collected to analyze oxidative stress and inflammation parameters before surgery and on the first and seventh days postoperatively. Serum concentrations of MDA, SOD, GPX, CAT, IL-1, IL-6, and CRP were measured using coated enzyme-linked immunosorbent assay (ELISA) kits. EORTC QLQ-H&H43 questionnaire was used to measure the QOL of patients. (3) Results and Conclusions: T stage, pain intensity, and the extent of the surgical procedure were established as significant predictive factors for QOL in multivariate analysis. There was a significant positive correlation between surgical complication occurrence and preoperative values of GPX and MDA, but significant predictors of surgical complication occurrence on the 7th postoperative day were SOD and MDA values (p < 0.05). Full article
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24 pages, 4683 KiB  
Article
Polyphenolic Compounds Activate SERCA1a and Attenuate Methylglyoxal- and Palmitate-Induced Impairment in Pancreatic INS-1E Beta Cells
by Vladimir Heger, Barbora Benesova, Magdalena Majekova, Petronela Rezbarikova, Attila Hunyadi, Lubica Horakova and Jana Viskupicova
Cells 2024, 13(22), 1860; https://doi.org/10.3390/cells13221860 - 9 Nov 2024
Cited by 1 | Viewed by 1664
Abstract
Sarco/endoplasmic reticulum Ca2+-ATPase (SERCA) is an important regulatory protein responsible for maintaining calcium homeostasis within cells. Impairment of SERCA associated with activity/expression decrease has been implicated in multiple chronic conditions, including cardiovascular diseases, diabetes, cancer, neurodegenerative diseases, and skeletal muscle pathologies. [...] Read more.
Sarco/endoplasmic reticulum Ca2+-ATPase (SERCA) is an important regulatory protein responsible for maintaining calcium homeostasis within cells. Impairment of SERCA associated with activity/expression decrease has been implicated in multiple chronic conditions, including cardiovascular diseases, diabetes, cancer, neurodegenerative diseases, and skeletal muscle pathologies. Natural polyphenols have been recognized to interact with several target proteins involving SERCA. To date, only a limited number of polyphenolic compounds or their derivatives have been described either to increase SERCA activity/expression directly or to affect Ca2+ signaling pathways. In this study, we tested polyphenols for their ability to activate SERCA1a in the absence or presence of methylglyoxal or palmitate and to impact insulin release in pancreatic beta cells. The protective effects of these compounds against methylglyoxal- or palmitate-induced injury were evaluated. Results indicate that 6-gingerol, resveratrol, and ellagic acid activate SERCA1a and protect against activity decrease induced by methylglyoxal and palmitate. Molecular docking analysis revealed the binding of these polyphenols to Glu439 in the SERCA1a P-domain, suggesting a critical role in the stimulation of enzyme activity. Ellagic acid was found to directly stimulate the activity of SERCA1a, marking the first instance of such an observation. Full article
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