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Innovative Strategies to Target Metabolism, Inflammation, and Oxidative Stress in Human Diseases

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (20 August 2025) | Viewed by 14196

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Dr. Kota V. Ramana

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Department of Biomedical Sciences, Noorda College of Osteopathic Medicine, Provo, UT 84606, USA
Interests: oxidative stress-induced signal transduction mechanisms; pathophysiology of secondary diabetic complications; carcinogenesis; inflammatory complications; therapeutic development of small molecular inhibitors and antioxidants
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Special Issue Information

Dear Colleagues,

Interfering with metabolism, inflammation, and oxidative stress is essential for managing various human diseases. Numerous recent studies have demonstrated strong links between cellular metabolism, inflammation, and oxidative stress, which contribute to the pathophysiology of conditions such as diabetes, aging, cardiovascular diseases, neurological disorders, and cancer. Strategies targeting these processes could offer therapeutic benefits. Specifically, dietary interventions, pharmacological agents, anti-inflammatory drugs, and lifestyle modifications like regular exercise and stress reduction can help control disease development and progression. Additionally, nutritional supplements, natural antioxidants, and phytochemicals that regulate various molecular signaling pathways may play crucial preventive roles in disease control. Emerging therapies, including gene editing, stem cell therapy, next-generation sequencing, regenerative medicine, and microbiome manipulation, show promise in modulating cellular metabolism, inflammatory responses, and oxidative stress for future treatments.

This Special Issue aims to provide an updated overview of the complex interplay between metabolic imbalance, chronic inflammation, and oxidative stress in the pathophysiology of human diseases. It invites contributions in the form of structural and computational studies, functional analyses, preclinical and clinical research, and comprehensive reviews, focusing on novel strategies targeting metabolism, inflammation, and oxidative stress to control various human pathologies.

Dr. Kota V. Ramana
Guest Editor

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Keywords

metabolism
inflammation
oxidative stress
diabetes
aging
cardiovascular diseases
gene editing
stem cell therapy
next-generation sequencing
regenerative medicine

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Published Papers (11 papers)

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Research

Jump to: Review

21 pages, 2210 KB

Open AccessArticle

Thiamine Compounds Alleviate Oxidative Stress, Over-Expression of Pro-Inflammatory Markers and Behavioral Abnormalities in a Mouse Predation Model of PTSD

by Tatyana Strekalova, Anna Gorlova, Joao Costa-Nunes, Aleksandr Litavrin, Johannes P. M. de Munter, Alexei Lyundup, Aleksei Umriukhin, Andrey Proshin, Allan V. Kalueff, Edna Grünblatt and Susanna Walitza

Int. J. Mol. Sci. 2025, 26(14), 6627; https://doi.org/10.3390/ijms26146627 - 10 Jul 2025

Viewed by 596

Abstract

Experiences of life-threatening stimuli can induce post-traumatic stress disorder (PTSD), which is associated with long-lasting behavioral and neurochemical abnormalities. Despite its increased global incidence, the current treatment options for PTSD remain limited, highlighting the need for novel therapeutic strategies. As oxidative stress and neuroinflammation contribute to PTSD, the use of powerful antioxidants such as thiamine (B1 vitamin) compounds may counteract disease development. Young C57BL/6 mice received thiamine or benfotiamine in drinking water (each at a dose of 200 mg/kg/day) for 21 days, and for the last five days, they were subjected to rat exposure. Mice were studied for anxiety-like behavior, exploration, locomotion, grooming, social interactions, pain sensitivity, brain changes in protein carbonyl (PC), total glutathione (TG), and gene expression of distress and inflammation markers. Rat exposure induced anxiety-like behavior, excessive grooming, and alteration in locomotion, along with other abnormalities. Stressed, untreated mice had elevated levels of PC and TG in the prefrontal cortex, hippocampus, amygdala, and striatum and increased expression of Il-1β, Tnf, c-Fos, Cox-1, and Cox-2. Treatment with thiamine or benfotiamine significantly ameliorated most of these changes in the stressed groups. Thus, thiamine compounds may have therapeutic potential in patients with PTSD, owing to their antioxidant and anti-inflammatory properties. Full article

(This article belongs to the Special Issue Innovative Strategies to Target Metabolism, Inflammation, and Oxidative Stress in Human Diseases)

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10 pages, 1121 KB

Open AccessArticle

In Experimental Tuberculosis Infection, the Bacteriostatic Function of Macrophages Is Activated by Th1 CD4⁺ T-Effectors in a Nitrite-Independent Manner

by Vladimir V. Evstifeev, Konstantin B. Majorov, Vadim G. Avdienko, Vladimir V. Yeremeev and Galina S. Shepelkova

Int. J. Mol. Sci. 2025, 26(14), 6573; https://doi.org/10.3390/ijms26146573 - 8 Jul 2025

Viewed by 429

Abstract

The pivotal component in the protection against TB is the tissue macrophages (Mф). These cells have been demonstrated to play a crucial role in the elimination of pathogens and mycobacterial killing. Elucidation of the molecular and phenotypic events that determine the outcome of infection in Mф is fundamental to understanding the key features of these cells that are so important in fighting infection. Mф activation is driven by cytokines and other inflammatory mediators secreted by T lymphocytes. The interaction between Mycobacterium tuberculosis (Mtb) and host Мф has been the subject of extensive in vitro research. This dynamic interplay represents a pivotal step in the progression of mycobacterial infection because pulmonary macrophages constitute the primary line of defense against the pathogen, thereby serving as the initial immune cells to which Mtb must adapt to establish a replicative foothold within the host. Our studies have demonstrated that highly differentiated Th1 effectors with the CD27^low phenotype exhibit superior efficacy in activating both peritoneal (Mф: T cell ratio ranging from 125:1 to 625:1) and pulmonary macrophages (Mф: T cell ratio = 5:1) compared to cells with the CD27^high phenotype. Furthermore, our findings indicate that this activation mechanism is not contingent upon the production of reactive nitrogen species. To effectively activate the bacteriostatic function of macrophages, CD27^high T lymphocytes must differentiate into effectors with the CD27^low phenotype. Full article

(This article belongs to the Special Issue Innovative Strategies to Target Metabolism, Inflammation, and Oxidative Stress in Human Diseases)

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17 pages, 3309 KB

Open AccessArticle

Mitochondrial Fragmentation and Long Noncoding RNA MALAT1 in Diabetic Retinopathy

by Renu A. Kowluru and Jay Kumar

Int. J. Mol. Sci. 2025, 26(13), 6429; https://doi.org/10.3390/ijms26136429 - 3 Jul 2025

Viewed by 581

Abstract

Mitochondria are dynamic in nature and depending on the energy demand they fuse and divide. This fusion-fission process is impaired in diabetic retinopathy and the promoter DNA of Mfn2, a fusion gene, is hypermethylated and its expression is downregulated. Long noncoding RNAs (RNAs with >200 nucleotides that do not encode proteins) can regulate gene expression by interacting with DNA, RNA, and proteins. Several LncRNAs are aberrantly expressed in diabetes, and among them, MALAT1 is upregulated in the retina, altering the expression of the genes associated with inflammation. Our aim was to investigate MALAT1’s role in mitochondrial dynamics in diabetic retinopathy. Using MALAT1-siRNA-transfected human retinal endothelial cells (HRECs) and human retinal Muller cells (RMCs) incubated in 20 mM D-glucose, Mfn2 expression and activity and its promoter DNA methylation were quantified. Mitochondrial integrity was evaluated by analyzing their fragmentation, ultrastructure, membrane potential, and oxygen consumption rate. Compared to normal glucose, high glucose upregulated MALAT1 expression and downregulated Mfn2 expression and activity in both HRECs and RMCs. MALAT1-siRNA ameliorated the glucose-induced increase in Mfn2 promoter DNA hypermethylation and its activity. MALAT1-siRNA also protected against mitochondrial fragmentation, structural damage, and reductions in the oxygen consumption rate. In conclusion, the upregulation of MALAT1 in diabetes facilitates Mfn2 promoter DNA hypermethylation in retinal vascular and nonvascular cells, leading to its suppression and the accumulation of the fragmented/damaged mitochondria. Thus, the regulation of MALAT1 has the potential to protect mitochondria and provide a possible new target to inhibit/prevent the blinding disease in diabetic patients. Full article

(This article belongs to the Special Issue Innovative Strategies to Target Metabolism, Inflammation, and Oxidative Stress in Human Diseases)

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14 pages, 1156 KB

Open AccessArticle

Repeated Valproic Acid Administration Fundamentally Ameliorated Cisplatin-Induced Mechanical Allodynia in Rats

by Yoshihiro Seto, Yuki Ohara, Manami Tachi, Mari Tomonari, Daisuke Inoue, Fumiyasu Okazaki, Yasuhiro Tsuji and Hideto To

Int. J. Mol. Sci. 2025, 26(11), 4977; https://doi.org/10.3390/ijms26114977 - 22 May 2025

Viewed by 477

Abstract

Cisplatin (cis-diamminedichloro-platinum; CDDP) is a chemotherapeutic agent that frequently induces peripheral neuropathy characterized by mechanical allodynia. Herein, we aimed to determine the effects of valproic acid (VPA) on cisplatin-induced mechanical allodynia in rats and elucidate the underlying mechanisms. A single administration of VPA (150 mg/kg) transiently suppressed CDDP-induced mechanical allodynia, correlating with serum VPA concentrations. Repeated VPA administration before or after the onset of CDDP-induced mechanical allodynia significantly attenuated allodynia even after VPA discontinuation, suggesting fundamental treatment potential. Mechanistically, CDDP increased the expression of neurokinin 1 receptor (NK1R) mRNA in the dorsal horn of the spinal cord, and this increased expression was suppressed by repeated VPA administration. Treatment with an NK1R antagonist alleviated CDDP-induced mechanical allodynia, indicating the involvement of NK1R in allodynia. In vitro assays revealed that VPA did not affect the cytotoxicity of CDDP in Walker 256 cells, suggesting that VPA does not interfere with the antitumor activity of CDDP. Overall, repeated VPA administration may fundamentally ameliorate CDDP-induced peripheral neuropathy by suppressing the CDDP-induced increased NK1R expression without compromising the antitumor effects of CDDP. These findings provide insights into the potential use of VPA as a therapeutic agent for managing CDDP-induced peripheral neuropathy. Full article

(This article belongs to the Special Issue Innovative Strategies to Target Metabolism, Inflammation, and Oxidative Stress in Human Diseases)

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20 pages, 1905 KB

Open AccessArticle

Salivary Zinc and Copper Levels Are Differentially Associated with ROS Levels in Breast Cancer Patients

by Elena I. Dyachenko, Elena A. Sarf and Lyudmila V. Bel’skaya

Int. J. Mol. Sci. 2025, 26(10), 4784; https://doi.org/10.3390/ijms26104784 - 16 May 2025

Viewed by 638

Abstract

Disruption of the balanced metabolism of copper and zinc can be both a consequence and potential cause-trigger for the occurrence of many pathological conditions including cancer. Zinc is an important cofactor of many enzymes that participate in inflammatory and redox reactions and the immune response, and refers to the components of DNA transcription factors. Copper plays an important role in processes such as cuproplasia and cuproptosis, affecting the process of cell differentiation and the epithelial–mesenchymal transition of cancer cells. In this regard, the study of changes in copper and zinc in breast cancer can provide valuable information on the metabolic features of cancer cells. In this study, we investigated the metabolic relationship between the zinc and copper levels in the saliva of patients with breast cancer and the content of reactive oxygen species, the state of the antioxidant and immune systems as well as the metabolism of the amino acids Cys, His, Met, and Arg. We also considered how the content and ratio of copper and zinc in saliva changes in patients with breast cancer depend on the state of the hormonal background and the expression of hormone receptors. Full article

(This article belongs to the Special Issue Innovative Strategies to Target Metabolism, Inflammation, and Oxidative Stress in Human Diseases)

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10 pages, 617 KB

Open AccessArticle

Aqueous Humor Cytokine Profiling Reveals Distinct Roles for Serum Amyloid A, Interleukin-8, and Endothelin-1 in Pseudoexfoliation Syndrome and Glaucoma

by Yoichi Kadoh, Yuji Takayanagi, Kazunobu Sugihara, Sachiko Kaidzu, Yasuyuki Takai and Masaki Tanito

Int. J. Mol. Sci. 2025, 26(4), 1461; https://doi.org/10.3390/ijms26041461 - 10 Feb 2025

Cited by 1 | Viewed by 980

Abstract

Pseudoexfoliation syndrome (PE), which is often unilateral in 60% of cases, is a risk for exfoliation glaucoma (EXG) with elevated inflammatory cytokines. This study aimed to clarify the dynamics of these cytokines in unilateral PE (u-PE) patients. This study included 20 eyes from 10 u-PE patients (PE+ eyes and fellow PE− eyes) and 20 eyes from 10 cataract patients without PE (control group). Clinical parameters, including age, visual acuity, and intraocular pressure, were assessed. Anterior chamber aqueous humor cytokine levels (IL-8, SAA, ET-1, VEGF) were measured and compared among groups. SAA was elevated in PE+ eyes compared to PE− and control eyes. IL-8 and ET-1 were elevated in both PE+ and PE− eyes compared to controls. IL-8 was associated with worsening visual acuity, while ET-1 correlated inversely. Our findings suggest that SAA is associated with the manifest disease while IL-8 and ET-1 could be early biomarkers for PE and therapeutic targets to prevent glaucomatous damage, as these markers appear in the aqueous humor even before pseudoexfoliation material becomes clinically evident. These results may enable earlier diagnosis and therapeutic intervention before the clinical onset of PE in patients with risk factors. Full article

(This article belongs to the Special Issue Innovative Strategies to Target Metabolism, Inflammation, and Oxidative Stress in Human Diseases)

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Review

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21 pages, 848 KB

Open AccessReview

Food-Derived Phytochemicals: Multicultural Approaches to Oxidative Stress and Immune Response

by Eiger Gliozheni, Yusuf Salem, Eric Cho, Samuel Wahlstrom, Dane Olbrich, Brandon Shams, Michael Alexander and Hirohito Ichii

Int. J. Mol. Sci. 2025, 26(15), 7316; https://doi.org/10.3390/ijms26157316 - 29 Jul 2025

Viewed by 482

Abstract

This review will focus on how ethnic consumption of foods such as shiitake, ginseng, turmeric, black seeds, berries, rosemary, moringa and holy basil can help act as antioxidants and immune modulators in fighting many diseases. We will investigate how these foods act on pathways like Nrf2/Keap1 to increase endogenous antioxidant capacity and help in reducing ROS production, based on publications found in PubMed between 1994 and 2024. In addition, we will show how these plants can cause immune system shifts by changing the makeup of the ratio of Th1/Th2 cells, reduce inflammation, and have antiangiogenic effects on cancer. This review will also show how plants can alter the gut microbiota and lead to a further decrease in oxidative stress. Overall, it will show how plants and their metabolites can potentially create a path forward for creating novel therapeutic approaches and help lead to an improved redox balance, support immune function, and enhance long-term health outcomes. Full article

(This article belongs to the Special Issue Innovative Strategies to Target Metabolism, Inflammation, and Oxidative Stress in Human Diseases)

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19 pages, 1097 KB

Open AccessReview

The Role of Inflammation in Neurodegenerative Diseases: Parkinson’s Disease, Alzheimer’s Disease, and Multiple Sclerosis

by Justyna Fołta, Zuzanna Rzepka and Dorota Wrześniok

Int. J. Mol. Sci. 2025, 26(11), 5177; https://doi.org/10.3390/ijms26115177 - 28 May 2025

Viewed by 1539

Abstract

Neurodegenerative diseases are a group of conditions that have in common the progressive damage and degeneration of neurons in the central nervous system. This group includes Parkinson’s disease, Alzheimer’s disease, and multiple sclerosis, among others. In recent years, increasing evidence has pointed to the important role of inflammation in the pathogenesis of these conditions. The occurrence of inflammation in the brain, which is often triggered by pro-inflammatory activation of microglia or astrocytes, can consequently lead to a chronic inflammatory response that contributes to the development of neurodegenerative processes. Inflammatory processes themselves, both within the nervous system and throughout the human body, appear to be central to the initiation and progression of neuronal damage. Understanding the role of inflammation in these diseases may open up new perspectives and opportunities in the future in the development of effective therapies to improve patients’ quality of life as the vast majority of cases of patients affected by neurodegenerative diseases continue to be treated symptomatically since causal treatments are lacking. In this review, we provide information on the impact of inflammation on the pathogenesis, course, and potential therapeutic options for selected neurodegenerative diseases. In addition, this article provides a general description of neuroinflammation and the involvement and role of specific cells in the central nervous system. Full article

(This article belongs to the Special Issue Innovative Strategies to Target Metabolism, Inflammation, and Oxidative Stress in Human Diseases)

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25 pages, 1935 KB

Open AccessReview

From Nutrient to Nanocarrier: The Multifaceted Role of Vitamin B12 in Drug Delivery

by Nikita A. Kuldyushev, Sergey Y. Simonenko, Semen I. Goreninskii, Tatiana N. Pallaeva, Andrey A. Zamyatnin, Jr. and Alessandro Parodi

Int. J. Mol. Sci. 2025, 26(11), 5119; https://doi.org/10.3390/ijms26115119 - 26 May 2025

Viewed by 1839

Abstract

Vitamin B12 (B12), a crucial water-soluble vitamin, plays an essential role in various cellular functions, including DNA synthesis and cellular metabolism. This review explores recent advancements in B12 delivery systems and their potential applications in drug delivery. The unique absorption pathways of B12, which involve specific binding proteins and receptors, are highlighted, emphasizing the vitamin’s protective mechanisms that enhance its bioavailability. The review discusses the intricate multi-protein network involved in B12 metabolism and the implications of B12 deficiency, which can lead to significant health issues, including neurological and hematological disorders. Additionally, the potential of B12 as a drug carrier to improve the pharmacokinetic properties of poorly bioavailable medications is examined. The findings suggest that optimizing B12 delivery could enhance therapeutic outcomes in nanomedicine and other clinical applications. Full article

(This article belongs to the Special Issue Innovative Strategies to Target Metabolism, Inflammation, and Oxidative Stress in Human Diseases)

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19 pages, 1280 KB

Open AccessReview

Mitochondrial DNA in Exercise-Mediated Innate Immune Responses

by Xin Wen, Jingcheng Fan, Xuemei Duan, Xinyi Zhu, Jianzheng Bai and Tan Zhang

Int. J. Mol. Sci. 2025, 26(7), 3069; https://doi.org/10.3390/ijms26073069 - 27 Mar 2025

Viewed by 1113

Abstract

Mitochondria are considered as “the plant of power” with cells for a long time. However, recent researches suggest that mitochondria also take part in innate immune response to a great extent. Remarkably, mtDNA was reported to have immunnostimulatory potential in 2004. Since then, there has been rapid growth in understanding the role of mtDNA in innate immune. The mtDNA is released into cytosol, extracellular environment, or circulating blood through BAK/BAX pore, mPTP, and GSDMD pore upon mitochondrial damage, where it is recognized by PRRs including TLR9, cGAS, and NLRP3, thereby triggering innate immune response. On the other hand, regular exercise has been recognized as an effective intervention strategy for innate immune response. Some studies show that chronic moderate-intensity endurance exercise, resistance training, HIIT, and moderate-intensity acute exercise enhance mitochondrial function by promoting mtDNA transcription and replication, thus blunting the abnormal release of mtDNA and excessive innate immune response. On the contrary, high-intensity acute exercise elicits the opposite effect. Nevertheless, only a very small body of research by far has been performed to illustrate the impact of exercise on mtDNA-driven innate immune response, and an overall review is lacking. In light of these, we summarize the current knowledge on the mechanism mediating the release of mtDNA, the role of mtDNA in innate immune response and the influence of exercise on mtDNA leakage, hoping to pave the way to investigate new diagnostic and therapeutic approaches for immunopathies. Full article

(This article belongs to the Special Issue Innovative Strategies to Target Metabolism, Inflammation, and Oxidative Stress in Human Diseases)

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28 pages, 11548 KB

Open AccessReview

Molecular and Cellular Mechanisms Involved in the Pathophysiology of Retinal Vascular Disease—Interplay Between Inflammation and Oxidative Stress

by Jovana V. Srejovic, Maja D. Muric, Vladimir Lj. Jakovljevic, Ivan M. Srejovic, Suncica B. Sreckovic, Nenad T. Petrovic, Dusan Z. Todorovic, Sergey B. Bolevich and Tatjana S. Sarenac Vulovic

Int. J. Mol. Sci. 2024, 25(21), 11850; https://doi.org/10.3390/ijms252111850 - 4 Nov 2024

Cited by 17 | Viewed by 4499

Abstract

Retinal vascular diseases encompass several retinal disorders, including diabetic retinopathy, retinopathy of prematurity, age-related macular degeneration, and retinal vascular occlusion; these disorders are classified as similar groups of disorders due to impaired retinal vascularization. The aim of this review is to address the main signaling pathways involved in the pathogenesis of retinal vascular diseases and to identify crucial molecules and the importance of their interactions. Vascular endothelial growth factor (VEGF) is recognized as a crucial and central molecule in abnormal neovascularization and a key phenomenon in retinal vascular occlusion; thus, anti-VEGF therapy is now the most successful form of treatment for these disorders. Interaction between angiopoietin 2 and the Tie2 receptor results in aberrant Tie2 signaling, resulting in loss of pericytes, neovascularization, and inflammation. Notch signaling and hypoxia-inducible factors in ischemic conditions induce pathological neovascularization and disruption of the blood–retina barrier. An increase in the pro-inflammatory cytokines—TNF-α, IL-1β, and IL-6—and activation of microglia create a persistent inflammatory milieu that promotes breakage of the blood–retinal barrier and neovascularization. Toll-like receptor signaling and nuclear factor-kappa B are important factors in the dysregulation of the immune response in retinal vascular diseases. Increased production of reactive oxygen species and oxidative damage follow inflammation and together create a vicious cycle because each factor amplifies the other. Understanding the complex interplay among various signaling pathways, signaling cascades, and molecules enables the development of new and more successful therapeutic options. Full article

(This article belongs to the Special Issue Innovative Strategies to Target Metabolism, Inflammation, and Oxidative Stress in Human Diseases)

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