Cell Signaling and Redox Biology: From Molecular Mechanisms to Therapeutic Applications

Topic Information

Dear Colleagues,

Cell signaling events and pathways control a cell’s environmental perception and subsequent functioning. It is now apparent that redox biology is part of the suite of mechanisms which orchestrate signaling events in cells. Internally, the redox status of a cell is held at a reducing level and is finely controlled in a balanced manner. This is achieved by the presence of many small redox-active molecules, such as glutathione and ascorbate, but also by a number of dietary antioxidants, such as vitamin E, and by antioxidant enzymes such as superoxide dismutase and catalase. Numerous small reactive molecules can be generated, and their metabolism can maintain or disrupt the redox balance of cells. These include reactive oxygen species (ROS), such as hydrogen peroxide (H₂O₂), reactive nitrogen species (RNS), such as nitric oxide (NO), and reactive sulfur species (RSS), such as hydrogen sulfide (H₂S). Redox mechanisms can control the action of proteins through covalent modifications, for example, by S-nitrosylation, therefore controlling cellular activities. Cell growth, development, and death, for example, through apoptosis, can all be controlled, in part, by redox metabolism. Redox dysfunction has been associated with a range of stress responses and diseases, both in plants and animals. Redox events can be used in pathogen control, as well as cellular dysfunction, through nitro-oxidative stress. Diseases such as Parkinson’s, Alzheimer’s, and other neurodegenerative diseases often have an element of redox imbalance, as does diabetes. The aging process also involves redox metabolism. Therefore, an understanding of the molecular mechanisms of redox biology and how therapeutics and treatments can be used to manipulate cellular redox is important. This Topic aims to bring together an array of cutting-edge research articles on redox biology from a range of organisms, from plants and nematodes to humans. Papers may be primary research articles or reviews. Interdisciplinary research is particularly welcomed, as are opinion articles suggesting ways to navigate bottlenecks in the field.

Prof. Dr. John T. Hancock
Prof. Dr. Sergej M. Ostojic
Prof. Dr. Jiankang Liu
Dr. Juan de Dios Alché Ramírez
Topic Editors

Keywords

Participating Journals

Journal Name	Impact Factor	CiteScore	Launched Year	First Decision (median)	APC
Antioxidants antioxidants	6.6	12.4	2012	18.7 Days	CHF 2900	Submit
Biology biology	3.5	7.4	2012	16.8 Days	CHF 2700	Submit
Nitrogen nitrogen	2.3	2.8	2020	16.7 Days	CHF 1200	Submit
Oxygen oxygen	-	8.4	2021	26.7 Days	CHF 1200	Submit
Clinical Bioenergetics clinbioenerg	-	-	2025	15.0 days *	CHF 1000	Submit
Plants plants	4.1	7.6	2012	16.5 Days	CHF 2700	Submit
Biomedicines biomedicines	3.9	6.8	2013	21 Days	CHF 2600	Submit

* Median value for all MDPI journals in the second half of 2025.

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Published Papers (3 papers)

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All Antioxidants Biology Nitrogen Oxygen Clinical Bioenergetics Plants Biomedicines

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22 pages, 1390 KB  

Open AccessReview

Ferroptosis in Myocardial Fibrosis: Mechanisms and Therapeutic Insights

by Xuefeng Lin, Weijun Li, Jiahao Ye and Lin Li

Antioxidants 2026, 15(1), 70; https://doi.org/10.3390/antiox15010070 - 6 Jan 2026

Viewed by 543

Abstract

Myocardial fibrosis (MF) is a common pathological feature of diverse cardiac disorders and is a key driving factor of cardiac dysfunction. It is marked by excessive deposition of extracellular matrix (ECM) proteins, particularly collagen type I and III, and a prolonged activation of [...] Read more.

Myocardial fibrosis (MF) is a common pathological feature of diverse cardiac disorders and is a key driving factor of cardiac dysfunction. It is marked by excessive deposition of extracellular matrix (ECM) proteins, particularly collagen type I and III, and a prolonged activation of cardiac fibroblasts. However, the molecular drivers of this process remain undetermined. Ferroptosis is an iron-catalyzed, lipid-peroxidation-dependent mode of regulated cell death. Research indicates that ferroptosis is significantly involved in the onset and advancement of MF; consequently, developing therapies that selectively modulate ferroptosis presents a promising direction of treatment options. Therefore, this paper systematically discusses the mechanisms associated with ferroptosis to explore the link between ferroptosis and MF from multiple dimensions, including iron metabolism disorders, lipid peroxidation, imbalance of glutathione metabolism, and the dysregulated activation of ferroptosis regulatory pathways, to provide innovative perspectives for the study of the specific molecular mechanisms and treatment of MF. Method: By retrieving the literature on the mechanism of ferroptosis in MF published in PubMed and Web of Science databases from 2020 to July 2025, the mechanism of action was systematically analyzed and reviewed. Full article

(This article belongs to the Topic Cell Signaling and Redox Biology: From Molecular Mechanisms to Therapeutic Applications)

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21 pages, 7425 KB  

Open AccessArticle

Oxidative-Stress-Mediated AMPK/mTOR Signaling in Bovine Mastitis: An Integrative Analysis Combining 16S rDNA Sequencing and Molecular Pathology

by Yuanyuan Zhang, Min Zhang, Daqing Wang, Feifei Zhao, Luofei Jia, Zhiwei Sun, Guifang Cao and Yong Zhang

Biology 2026, 15(2), 115; https://doi.org/10.3390/biology15020115 - 6 Jan 2026

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Abstract

The bovine mammary gland, the exclusive site of milk synthesis, is a structurally specialized tissue that houses distinct cellular subsets, yet it remains highly susceptible to major mastitis pathogens, including Staphylococcus aureus, Streptococcus agalactiae, and Escherichia coli. Infection disrupts redox [...] Read more.

The bovine mammary gland, the exclusive site of milk synthesis, is a structurally specialized tissue that houses distinct cellular subsets, yet it remains highly susceptible to major mastitis pathogens, including Staphylococcus aureus, Streptococcus agalactiae, and Escherichia coli. Infection disrupts redox homeostasis, leading to excessive accumulation of reactive oxygen species (ROS) and rapid activation of antioxidant pathways. In this study, we integrated 16S DNA sequencing, histopathology (hematoxylin and eosin), and immunohistochemistry to map the mastitis-associated microbiota and visualize oxidative-damage foci in mammary tissues challenged by Staphylococcus aureus, Streptococcus agalactiae, or Escherichia coli. Quantitative reverse transcription polymerase chain reaction and Western blot analyses were subsequently performed on the same samples to measure the kinetic response of six oxidative-stress-related signalling nodes: adenosine 5′-monophosphate-activated protein kinase, cytochrome P450 1A1, heme oxygenase 1, nitric oxide synthase, mammalian target of rapamycin, and superoxide dismutase. By correlating the temporal expression patterns of these genes/proteins with ROS accumulation and histological severity, this study delineates the molecular cascade linking oxidative imbalance to mastitis pathology, providing data-driven targets for future preventive and therapeutic strategies. Full article

(This article belongs to the Topic Cell Signaling and Redox Biology: From Molecular Mechanisms to Therapeutic Applications)

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16 pages, 2307 KB  

Open AccessArticle

IL-1β Controls Proliferation, Apoptosis, and Necroptosis Through the PI3K/AKT/Src/NF-κB Pathway in Leukaemic Lymphoblasts

by Zitlal-Lin Victoria-Avila, Elba Reyes-Maldonado, María Lilia Domínguez-López, Jorge Vela-Ojeda, Aranza Lozada-Ruiz, Omar Rafael Alemán and Ruth Angélica Lezama

Biomedicines 2026, 14(1), 41; https://doi.org/10.3390/biomedicines14010041 - 24 Dec 2025

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Abstract

Background: Chronic inflammation and the development of cancer are closely linked, with components that comprise the tumour microenvironment—including proinflammatory cytokines—exerting essential tumourigenic effects. These proinflammatory cytokines include IL-1β, which has been reported to be overexpressed in several cancers and shown to activate several [...] Read more.

Background: Chronic inflammation and the development of cancer are closely linked, with components that comprise the tumour microenvironment—including proinflammatory cytokines—exerting essential tumourigenic effects. These proinflammatory cytokines include IL-1β, which has been reported to be overexpressed in several cancers and shown to activate several signalling pathways. These pathways may involve kinases such as AKT (serine/threonine kinase) and Src (Proto-oncogene tyrosine-protein kinase), and have a broad capacity to activate nuclear factors, including NF-κB (Nuclear Factor kappa-light-chain-enhancer of activated B cells), which can regulate the transcription of genes encoding proteins such as cIAP1 (Cellular Inhibitor of Apoptosis Protein 1), Bcl-2 (B-cell lymphoma 2), and cyclin D1, thereby regulating processes like apoptosis and cell cycle inhibition. Objectives: The aim of this study was to investigate the role of IL-1β (Interleukin-1 beta) in regulating cell death and proliferation in RS4:11 leukaemic lymphoblasts via the PI3K (Phosphoinositide 3-kinase)/AKT/Src/NF-κB pathway using an in vitro experimental approach. Methods: We employed flow cytometry to determine the expression levels and phosphorylation status of various proteins; proliferation was assessed using the CCK-8 kit, and apoptosis was evaluated with the Annexin V kit. Results: Our findings indicate that the IL-1β-activated signalling pathway modulates these cellular processes in leukaemic lymphoblasts. Conclusions: We therefore conclude that IL-1β exerts significant effects on cell death and proliferation in leukaemic lymphoblasts through the PI3K/AKT/NF-κB pathway, with the study’s findings indicating that an inflammatory environment may promote such lymphoblasts to acquire neoplastic characteristics. As such, the proteins involved in the effects evaluated in this work could be considered as potential therapeutic targets for the treatment of Acute Lymphoblastic Leukaemia (ALL). Full article

(This article belongs to the Topic Cell Signaling and Redox Biology: From Molecular Mechanisms to Therapeutic Applications)

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