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

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: 20 August 2025 | Viewed by 4940

Special Issue Editor

Dr. Kota V. Ramana

E-Mail Website
Guest Editor
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
Special Issues, Collections and Topics in MDPI journals

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

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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

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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 (3 papers)

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Research

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10 pages, 617 KiB  
Article
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 649
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 [...] Read more.
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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19 pages, 1280 KiB  
Review
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 419
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, [...] Read more.
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 KiB  
Review
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 8 | Viewed by 3170
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 [...] Read more.
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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