Oxidative Stress and Inflammation, 3rd Edition

Topic Information

Dear Colleagues,

Oxidative stress is viewed as an imbalance between the production of reactive oxygen species (ROS) and their elimination by protective mechanisms, which can lead to chronic inflammation. Certain lifestyles and the intake of external unhealthy chemicals are the major causes of age-related chronic diseases and cancer. Their study includes disease pathology pathways, lifestyle, treatment, protection, and prevention of oxidative stress and inflammation. ROS are normally produced within the body in limited amounts and are essential compounds involved in the regulation of processes that can maintain cell homeostasis and functions (signal transduction, gene expression, and activation of receptors). An imbalance may cause oxidative stress, which can lead to lipid peroxidation, gene mutation, inflammation, and other complications. The harmful oxidative activity of ROS can be only counteracted by antioxidant/anti-inflammatory compounds, which may be both synthetic and natural, but are often characterized by several stability issues, such as poor water solubility and low bioavailability, which compromise their in vivo activities. The aim of this Topic is to collect research papers providing an overview of the current status of research on both natural and synthetic products with antioxidant properties that can counteract inflammatory diseases, including, but not necessarily restricted to, chemical compounds (synthetic or of natural origin), vitamins, peptides, micronutrients, non-starch polysaccharides, probiotics, postbiotics, prebiotics formulations containing functional foods, nutraceutical or cosmeceutical products, and innovative oral, systemic, or topical delivery methods that are capable of overcoming their stability issues.

Dr. Maria Letizia Manca
Dr. Amparo Nacher
Dr. Matteo Perra
Dr. Ines Castangia
Dr. Mohamad Allaw
Topic Editors

Keywords

Participating Journals

Journal Name	Impact Factor	CiteScore	Launched Year	First Decision (median)	APC
Antioxidants antioxidants	6.6	12.4	2012	17.4 Days	CHF 2900	Submit
Biomedicines biomedicines	3.9	6.8	2013	17 Days	CHF 2600	Submit
International Journal of Molecular Sciences ijms	4.9	9.0	2000	20.5 Days	CHF 2900	Submit
Life life	3.4	6.0	2011	19.3 Days	CHF 2600	Submit
Oxygen oxygen	-	8.4	2021	24 Days	CHF 1000	Submit
Cosmetics cosmetics	3.2	6.0	2014	22.5 Days	CHF 1800	Submit
Nutraceuticals nutraceuticals	-	-	2021	32.7 Days	CHF 1000	Submit

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All Antioxidants Biomedicines IJMS Life Oxygen Cosmetics Nutraceuticals

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48 pages, 2461 KB  

Open AccessReview

Role of Matricellular Proteins in Endothelial Cell Inflammation and Atherosclerosis

by Ravi Varma Aithabathula, Santosh Kumar and Bhupesh Singla

Antioxidants 2025, 14(11), 1338; https://doi.org/10.3390/antiox14111338 - 6 Nov 2025

Viewed by 742

Abstract

The vascular endothelium serves as a critical barrier preventing the transmigration of monocytes, circulating lipoproteins, and other molecules into the subendothelial space, and plays a vital role in regulating vascular tone. A dysfunctional and inflamed endothelial layer in response to disturbed blood flow [...] Read more.

The vascular endothelium serves as a critical barrier preventing the transmigration of monocytes, circulating lipoproteins, and other molecules into the subendothelial space, and plays a vital role in regulating vascular tone. A dysfunctional and inflamed endothelial layer in response to disturbed blood flow or other proatherogenic risk factors is the initiating event in the pathogenesis of atherosclerosis, suggesting the importance of an intact and properly functioning endothelium in preventing the onset and progression of this disease. Accumulated evidence demonstrates the significant role of matricellular proteins, which are non-structural and secretory extracellular matrix (ECM) proteins, in the development of atherosclerosis. These proteins exert multifaceted effects on endothelial cells (ECs) ranging from reactive oxygen species (ROS) production, endoplasmic reticulum stress, and expression of adhesion molecules to autophagy and compromised barrier function via stimulating various molecular mechanisms. Given the critical roles of these processes in EC function and atherosclerosis, a better understanding of signaling pathways governed by matricellular proteins in ECs is required to develop therapeutic strategies for suppressing or preventing atherosclerosis and related cardiovascular diseases (CVDs). This review comprehensively summarizes the existing literature on the diverse roles of matricellular proteins in regulating EC inflammation and function, and highlights their potential as viable therapeutic targets for maintaining vascular health and inhibiting the progression of atherosclerosis. Full article

(This article belongs to the Topic Oxidative Stress and Inflammation, 3rd Edition)

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17 pages, 1319 KB  

Open AccessArticle

Oxidative Stress Score as an Indicator of Pathophysiological Mechanisms Underlying Cardiovascular Disease in Kidney Transplant Recipients

by Valera-Arévalo Gemma, Paula Jara Caro, María del Mar Rodríguez-San Pedro, Claudia Yuste, María Gabriela Ortiz-Diaz, Rafael Ramírez, Matilde Alique, Natalia Guerra-Pérez, Julia Carracedo and Enrique Morales

Oxygen 2025, 5(4), 20; https://doi.org/10.3390/oxygen5040020 - 16 Oct 2025

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Abstract

Chronic kidney disease is closely associated with an increased risk of cardiovascular disease. Although kidney transplantation represents the treatment of choice for patients with end-stage chronic kidney disease, it is also linked to significant cardiovascular risk. This study aimed to evaluate the relationship [...] Read more.

Chronic kidney disease is closely associated with an increased risk of cardiovascular disease. Although kidney transplantation represents the treatment of choice for patients with end-stage chronic kidney disease, it is also linked to significant cardiovascular risk. This study aimed to evaluate the relationship between cardiovascular pathology and oxidative status in kidney transplant recipients, while also assessing the influence of disease etiology and humoral immune response on oxidative imbalance. A cross-sectional analysis was conducted in individuals with advanced chronic kidney disease (n = 36) and kidney transplant recipients (n = 40). A total of 18 healthy subjects were included. The enzymatic activities of xanthine oxidase, superoxide dismutase, and glutathione peroxidase, and levels of lipid peroxidation products, oxidized glutathione, and reduced glutathione were measured using spectrophotometry in plasma and mononuclear and polymorphonuclear leukocytes isolated using Ficoll density gradients. Individual oxidative status was evaluated using OXYSCORE. Kidney transplantation was associated with a higher incidence of cardiovascular disease (p < 0.01) and increased levels of both prooxidant (p < 0.01) and antioxidant parameters (p < 0.01). Elevated OXYSCORE values were observed particularly in patients with nephroangiosclerosis, diabetic kidney disease, polycystic kidney disease (p < 0.05), and cardiovascular comorbidities (p < 0.001). Additionally, the presence of anti-graft antibodies correlated with higher oxidative scores. These findings suggest that OXYSCORE may serve as a potential indicator of cardiovascular damage in kidney transplant recipients. Full article

(This article belongs to the Topic Oxidative Stress and Inflammation, 3rd Edition)

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11 pages, 3848 KB  

Open AccessArticle

Preventive and Therapeutic Effects of Hydrogen-Generating Si-Based Agent on Pressure Ulcers in Mice

by Naoya Otani, Takaki Oue, Yuki Kobayashi, Hikaru Kobayashi, Koichi Tomita and Tateki Kubo

Biomedicines 2025, 13(10), 2475; https://doi.org/10.3390/biomedicines13102475 - 11 Oct 2025

Viewed by 504

Abstract

Objectives: As a known antioxidant, hydrogen has been useful for treating pressure ulcers. However, conventional methods of hydrogen administration have limitations with regard to dosage and continuity of hydrogen intake. This study evaluated the efficacy of a novel Si-containing agent that can [...] Read more.

Objectives: As a known antioxidant, hydrogen has been useful for treating pressure ulcers. However, conventional methods of hydrogen administration have limitations with regard to dosage and continuity of hydrogen intake. This study evaluated the efficacy of a novel Si-containing agent that can generate substantial quantities of hydrogen to treat pressure ulcers in an in vivo mouse model. Methods: The back skin and subcutaneous tissue of mice were compressed with magnets for 12 h. Changes in the ulcer area after release of compression, histological findings, degree of apoptosis, and expression levels for oxidative stress markers and inflammation-related cytokines were compared between mice fed a normal diet (control group) and those fed a 2.5 wt% Si-based diet (Si group). Results: The Si group had a significantly smaller ulcer area and shorter healing period than the control group. Moreover, inflammatory responses, apoptotic activity, and oxidative stress within the ulcer tissue were suppressed significantly in the Si group. Conclusions: Oral intake of the Si-based agent can potentially treat and prevent pressure ulcers by regulating apoptosis, oxidative stress, and inflammatory responses. Full article

(This article belongs to the Topic Oxidative Stress and Inflammation, 3rd Edition)

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16 pages, 4051 KB  

Open AccessArticle

Protective Effect of Exogenous Adenosine Triphosphate Against Ocular Toxicity of Linezolid in Rats

by Cenap Mahmut Esenulku, Ibrahim Cicek, Ahmet Mehmet Somuncu, Bulent Yavuzer, Esra Tuba Sezgin, Tugba Bal Tastan, Nurinisa Yücel, Ezgi Karatas and Halis Suleyman

Life 2025, 15(10), 1587; https://doi.org/10.3390/life15101587 - 11 Oct 2025

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Abstract

Linezolid, a synthetic antimicrobial agent, may induce oxidative damage in ocular tissues, particularly in the optic nerve. Adenosine triphosphate (ATP) is involved in the production of antioxidants that scavenge and neutralize reactive oxygen species. This study aims to evaluate the potential protective effect [...] Read more.

Linezolid, a synthetic antimicrobial agent, may induce oxidative damage in ocular tissues, particularly in the optic nerve. Adenosine triphosphate (ATP) is involved in the production of antioxidants that scavenge and neutralize reactive oxygen species. This study aims to evaluate the potential protective effect of exogenous ATP against linezolid-induced ocular damage in rats, in comparison with methylprednisolone. Wistar-type rats were divided into five groups as follows: healthy (HG), ATP-only (ATPG), linezolid-only (LZDG), ATP + linezolid (ATLDG), and methylprednisolone + linezolid groups (MPLDG). Oxidative stress markers, antioxidant biomarkers, and proinflammatory cytokines were analyzed in isolated ocular tissues. Optic nerve tissue was also evaluated histopathologically. Linezolid administration increased the oxidative stress marker MDA and the proinflammatory cytokine TNF-α, while decreasing antioxidant parameters such as tGSH, SOD and CAT in rat ocular tissues, compared to the healthy group. However, it did not significantly alter serum troponin I levels. Histopathological analysis revealed that linezolid induced oxidative damage and inflammation in optic nerve tissue, with marked glial alterations. ATP administration reduced linezolid-induced oxidative stress in ocular tissue, as indicated by decreased MDA levels. It also enhanced antioxidant defenses by increasing tGSH, SOD, and CAT levels. In addition, ATP lowered proinflammatory cytokine levels, thereby alleviating inflammation. These effects collectively contributed to the restoration of biochemical parameters toward normal levels. In addition, ATP mitigated linezolid-induced optic nerve damage and glial alterations. The critical role of ATP in reducing oxidative stress, restoring antioxidant balance, and suppressing inflammation may represent a promising therapeutic approach for linezolid-induced ocular toxicity. Full article

(This article belongs to the Topic Oxidative Stress and Inflammation, 3rd Edition)

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18 pages, 3287 KB  

Open AccessArticle

In Silico and In Vitro Studies of Anti-Inflammatory, Anti-Oxidative Stress, and Anti-Apoptosis Effect of 7-Octenoic Acid Derived from Moringa oleifera Lam., on LPS-Induced Monocyte-Derived Macrophages (MDM)

by Kittipong Srimuang, Watunyoo Buakaew, Yordhathai Thongsri, Krai Daowtak, Pachuen Potup, Antonio Ferrante and Kanchana Usuwanthim

Int. J. Mol. Sci. 2025, 26(18), 8911; https://doi.org/10.3390/ijms26188911 - 12 Sep 2025

Viewed by 1532

Abstract

While Moringa oleifera Lam. (MO) extracts are known to have various bioactive properties, including anti-inflammatory properties, the components responsible still remain to be identified. This study explores the protective effects of the MO component, 7-octenoic acid (7OCT) in LPS-stimulated THP-1 macrophage inflammatory responses. [...] Read more.

While Moringa oleifera Lam. (MO) extracts are known to have various bioactive properties, including anti-inflammatory properties, the components responsible still remain to be identified. This study explores the protective effects of the MO component, 7-octenoic acid (7OCT) in LPS-stimulated THP-1 macrophage inflammatory responses. The compound significantly downregulated the production of the pro-inflammatory cytokines TNF-α, IL-1β, and IL-6, as well as the expression of inflammation-related genes NFKB1, PTGS2, and NOS2. Additionally, it inhibited the nuclear translocation of NF-κB p65, a key transcription factor of inflammatory signaling cascade. Effects on oxidative stress showed that 7OCT inhibited LPS-induced NADPH oxidase 2 (NOX2) component genes including CYBB, CYBA, NCF1, NCF2, and NFE2L2, along with phosphorylated NOX2 and p47^phox proteins. The compound reduced the expression of TP53, BAX, CASP3, and CASP7, while enhancing BCL2 expression and Bcl-2 protein levels, suggesting an effect on apoptosis. Decreased levels of BAX, caspase-3, and cleaved caspase-3 proteins further confirmed its anti-apoptotic effect. Our findings suggest that 7OCT exhibits strong anti-inflammatory, antioxidant, and anti-apoptotic properties. Full article

(This article belongs to the Topic Oxidative Stress and Inflammation, 3rd Edition)

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