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Molecular Mechanisms and Therapeutic Targeting of Inflammatory Complications
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Molecular Mechanisms and Therapeutic Targeting of Inflammatory Complications

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: 30 November 2025 | Viewed by 5934

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,

Inflammation is the body’s natural immune response to injury or infection, but it can lead to harmful inflammatory complications when it becomes chronic or dysregulated. The persistent activation of immune pathways, oxidative stress, and the impaired resolution of inflammation contribute to tissue damage, fibrosis, and organ dysfunction. These processes underlie a wide range of human inflammatory disorders. This Special Issue aims to provide an overview of the complex interplay between metabolic imbalance, chronic inflammation, and oxidative stress in the pathophysiology of human diseases, including, but not limited to, autoimmune diseases, infectious diseases, respiratory complications, metabolic disorders, cardiovascular disease, neuroinflammation, and cancer. We invite original research articles, reviews, case reports, and perspectives that explore cutting-edge research and emerging trends, seeking to help generate a deeper understanding of inflammation and promote the development of targeted and more effective therapies for inflammation-driven diseases. Specific topics of interest include

  • The cellular and molecular signaling pathways involved in inflammation;
  • The genetic and epigenetic regulation of inflammatory responses;
  • The interplay between immune cells and tissue microenvironments in inflammatory pathologies;
  • Biomarkers for the early detection, monitoring, and prognosis of inflammation-related complications;
  • Novel therapeutic strategies, including small molecules, antioxidants, biologics, nanomedicine, and gene therapies, targeting inflammatory pathways and complications;
  • Preclinical and clinical studies focused on modulating inflammation to prevent or treat  inflammatory pathologies.

Dr. Kota V. Ramana
Guest Editor

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Keywords

  • inflammation
  • oxidative stress
  • cytokines
  • autoimmune diseases
  • infectious diseases
  • cancer
  • targeted therapies
  • molecular pathways
  • asthma
  • sepsis

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Published Papers (4 papers)

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Research

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15 pages, 886 KB  
Article
Lymphocyte Phenotypes and Protein-Bound Uremic Toxins as Determinants of Clinical Outcomes in Hemodialysis Patients
by Theodoros Tourountzis, Georgios Lioulios, Stamatia Stai, Steven Van Laecke, Eleni Moysidou, Michalis Christodoulou, Ariadni Fouza, Asimina Fylaktou, Konstantia Kantartzi, Griet Glorieux and Maria Stangou
Int. J. Mol. Sci. 2025, 26(21), 10376; https://doi.org/10.3390/ijms262110376 (registering DOI) - 24 Oct 2025
Abstract
The impact of protein bound uremic toxins (PBUTs) and lymphocyte alterations in morbidity and mortality in patients on hemodialysis (HD) is of great concern. The aim of this study was the assessment of association between PBUTs, immunosenescent lymphocytes’ phenotype and clinical events [cardiovascular, [...] Read more.
The impact of protein bound uremic toxins (PBUTs) and lymphocyte alterations in morbidity and mortality in patients on hemodialysis (HD) is of great concern. The aim of this study was the assessment of association between PBUTs, immunosenescent lymphocytes’ phenotype and clinical events [cardiovascular, severe infections (hospitalization due to infection, respiratory infection), all-cause mortality] during 2-year follow-up. In this prospective observational study, lymphocytes’ phenotype of 54 patients on HD and 31 age-matched controls was analyzed by flow cytometry, and simultaneously, PBUT serum levels [hippuric acid (HA), indoxyl sulfate (IxS), p-cresyl sulfate (pCS), p-cresyl glycuronide (pCG), in-dole-3-acetic acid (IAA), and 3-carboxy-4-methyl-5-propyl-2-furanpropionate (CMPF)] were quantified by ultra-performance liquid chromatography. Patients with increased levels of free IxS and total and free HA had higher mortality within a 2-year follow-up period (p = 0.049, p = 0.01, p = 0.01, respectively). In patients who experienced cardiovascular events, higher concentrations of CMPF (p = 0.015) were observed. Higher total and free HA levels associate with increased all-cause mortality in patients on HD, independently of age, dialysis vintage, and decreased count of CD4+CD45RA+CD31+ and naïve B cells (CD19+IgD+CD27−). In patients on HD, increased levels of total and free HA associate with an increased risk of death. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Therapeutic Targeting of Inflammatory Complications)

Review

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21 pages, 1260 KB  
Review
COVID-19 Hijacking of the Host Epigenome: Mechanisms, Biomarkers and Long-Term Consequences
by Alena D. Zolotarenko, Hakob M. Poghosyan, Victoria V. Sheptiy and Sergey A. Bruskin
Int. J. Mol. Sci. 2025, 26(21), 10372; https://doi.org/10.3390/ijms262110372 (registering DOI) - 24 Oct 2025
Abstract
The epigenetics of COVID-19 is a rapidly expanding field that reveals how the SARS-CoV-2 virus initiates alterations in the host’s genome, influencing the susceptibility to infection, the disease severity, and long-term consequences, known as “long COVID.” In this review, we describe the mechanisms [...] Read more.
The epigenetics of COVID-19 is a rapidly expanding field that reveals how the SARS-CoV-2 virus initiates alterations in the host’s genome, influencing the susceptibility to infection, the disease severity, and long-term consequences, known as “long COVID.” In this review, we describe the mechanisms utilized by the virus to manipulate the host epigenome, suppressing antiviral responses and creating a favorable environment for viral replication. We also highlight virus-induced epigenetic changes across diverse cell populations that contribute to COVID-19 pathogenesis. Notably, the virus reprograms hematopoietic stem and progenitor cells, leading to long-lasting alterations in innate immunity, a phenomenon known as “trained immunity.” These epigenetic modifications are maintained in differentiated daughter cells and may explain the persistent inflammation and other symptoms of long COVID. Furthermore, we discuss emerging epigenetic biomarkers of disease severity, including methylation signatures in genes such as AIM2, HLA-C, and PARP9, as well as dysregulated miRNA profiles. Understanding this complex interplay between the virus and the host’s epigenetic landscape is crucial for developing new therapeutic approaches that target specific epigenetic modifications to suppress pathological processes and improve clinical outcomes for COVID-19 patients. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Therapeutic Targeting of Inflammatory Complications)
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36 pages, 3153 KB  
Review
Curcumin in Inflammatory Complications: Therapeutic Applications and Clinical Evidence
by Amber Zafar, Divya Lahori, Aleeza F. Namit, Zackery Paxton, Neha Ratna, Dallin Thornton and Kota V. Ramana
Int. J. Mol. Sci. 2025, 26(19), 9366; https://doi.org/10.3390/ijms26199366 - 25 Sep 2025
Viewed by 2860
Abstract
Curcumin is a diarylheptanoid polyphenol compound derived from the plant species Curcuma longa. For thousands of years, it has been used as a dietary supplement, food coloring agent, and natural antibiotic in many Asian countries. Recent studies have also investigated its potential [...] Read more.
Curcumin is a diarylheptanoid polyphenol compound derived from the plant species Curcuma longa. For thousands of years, it has been used as a dietary supplement, food coloring agent, and natural antibiotic in many Asian countries. Recent studies have also investigated its potential therapeutic role in a variety of inflammatory diseases, including osteoarthritis, asthma, chronic obstructive pulmonary disease, atherosclerosis, irritable bowel syndrome, sepsis, atopic dermatitis, and psoriasis. Although individual studies have reported beneficial effects, a comprehensive discussion on findings across these conditions has been lacking. This review systematically evaluates the therapeutic potential of curcumin in inflammatory diseases. Literature was sourced through a PubMed search using relevant terms such as curcumin, treatment, and the names of each targeted disease over the past two decades. We discussed the key findings on how curcumin administration was associated with improvements in disease markers, symptom relief, or progression delay. Despite promising research outcomes, the current evidence underscores the need for more robust, large-scale studies to confirm these effects and guide the clinical applications of curcumin in managing inflammatory disorders. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Therapeutic Targeting of Inflammatory Complications)
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37 pages, 4312 KB  
Review
Neutrophils and NETs in Pathophysiology and Treatment of Inflammatory Bowel Disease
by Marina Ortega-Zapero, Raquel Gomez-Bris, Ines Pascual-Laguna, Angela Saez and Jose M. Gonzalez-Granado
Int. J. Mol. Sci. 2025, 26(15), 7098; https://doi.org/10.3390/ijms26157098 - 23 Jul 2025
Viewed by 2846
Abstract
Inflammatory Bowel Disease (IBD), which includes ulcerative colitis (UC) and Crohn’s disease (CD), results from dysregulated immune responses that drive chronic intestinal inflammation. Neutrophils, as key effectors of the innate immune system, contribute to IBD through multiple mechanisms, including the release of reactive [...] Read more.
Inflammatory Bowel Disease (IBD), which includes ulcerative colitis (UC) and Crohn’s disease (CD), results from dysregulated immune responses that drive chronic intestinal inflammation. Neutrophils, as key effectors of the innate immune system, contribute to IBD through multiple mechanisms, including the release of reactive oxygen species (ROS), pro-inflammatory cytokines, and neutrophil extracellular traps (NETs). NETs are web-like structures composed of DNA, histones, and associated proteins including proteolytic enzymes and antimicrobial peptides. NET formation is increased in IBD and has a context-dependent role; under controlled conditions, NETs support antimicrobial defense and tissue repair, whereas excessive or dysregulated NETosis contributes to epithelial injury, barrier disruption, microbial imbalance, and thrombotic risk. This review examines the roles of neutrophils and NETs in IBD. We summarize recent single-cell and spatial-omics studies that reveal extensive neutrophil heterogeneity in the inflamed gut. We then address the dual role of neutrophils in promoting tissue damage—through cytokine release, immune cell recruitment, ROS production, and NET formation—and in supporting microbial clearance and mucosal healing. We also analyze the molecular mechanisms regulating NETosis, as well as the pathways involved in NET degradation and clearance. Focus is given to the ways in which NETs disrupt the epithelial barrier, remodel the extracellular matrix, contribute to thrombosis, and influence the gut microbiota. Finally, we discuss emerging therapeutic strategies aimed at restoring NET homeostasis—such as PAD4 inhibitors, NADPH oxidase and ROS pathway modulators, and DNase I—while emphasizing the need to preserve antimicrobial host defenses. Understanding neutrophil heterogeneity and NET-related functions may facilitate the development of new therapies and biomarkers for IBD, requiring improved detection tools and integrated multi-omics and clinical data. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Therapeutic Targeting of Inflammatory Complications)
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