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Molecular Mechanisms and Therapeutic Targeting of Inflammatory Complications

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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: 20 June 2026 | Viewed by 22148

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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,

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 (10 papers)

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Research

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13 pages, 932 KB

Open AccessArticle

Enterolignans Improve the Expression of Iron-Related Genes in a Cellular Model of Inflammatory Bowel Disease

by Ottavia Bonuccelli, Anna Gogna, Stefania Mitola, Giulia Abate, Fabiana Ferrari, Francesco Bertagna, Maria Antonia De Francesco, Eugenio Monti, Roberto Bresciani and Giorgio Biasiotto

Int. J. Mol. Sci. 2025, 26(22), 11153; https://doi.org/10.3390/ijms262211153 - 18 Nov 2025

Viewed by 404

Abstract

Anemia is the most common extraintestinal comorbidity of inflammatory bowel diseases (IBDs). Inflammatory cytokines are produced and exert their effects within the bowel microenvironment of IBD patients and, among them, Interleukin 6 (IL-6) induces the expression of hepcidin, encoded by the HAMP gene, contributing to the development of anemia. Enterodiol (END) and Enterolactone (ENL) are enterolignans that are known for their nutraceutical, anti-inflammatory, anti-oxidant, and estrogenic properties. Here, we used the Caco-2 cell line as an in vitro model of bowel disease to evaluate the potential nutraceutical effects of enterolignans on iron metabolism under an inflammatory stimulus induced by IL-6. As is known, IL-6 treatment induces the upregulation of HAMP gene expression. Notably, both END and ENL showed a pronounced anti-inflammatory effect, lowering HAMP mRNA levels and partially counteracting the effect induced by IL-6. The expression of iron-related genes was also studied to evaluate the effects on iron metabolism. IL-6 downregulated the expression of almost all genes studied. Notably, END and ENL mitigated the effect of IL-6, ameliorating the expression level of HAMP, FTH1, and ACO1, in addition to other END- or ENL-specific effects. The results of this study evidenced the interesting anti-inflammatory properties of enterolignans, which improved the iron homeostasis during inflammation, suggesting a possible role in the management of IBD patients with anemia. Full article

(This article belongs to the Special Issue Molecular Mechanisms and Therapeutic Targeting of Inflammatory Complications)

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16 pages, 2169 KB

Open AccessArticle

The Anti-Inflammatory and Skin Barrier Function Recovery Effects of Carica papaya Peel in Mice with Contact Dermatitis

by Seonah Park, Kyoungmin Sun, Yeojin Kim, Hyorhan Son, Jimi Lee, Soyeon Kim and Hyungwoo Kim

Int. J. Mol. Sci. 2025, 26(22), 11122; https://doi.org/10.3390/ijms262211122 - 17 Nov 2025

Viewed by 874

Abstract

With growing concerns over the safety of synthetic substances, the development of plant-derived alternatives with minimal adverse effects has gained significant attention. Carica papaya L. peel contains a rich profile of bioactive compounds, including papain, flavonoids, and vitamin C, which exhibit potent antioxidant and anti-inflammatory properties. This study aimed to evaluate the effects of an ethanol extract of C. papaya peel (EECP) on inflammation and skin barrier dysfunction in a mouse model of contact dermatitis (CD) induced by 1-fluoro-2,4-dinitrofluorobenzene (DNFB). Mice were treated by applying EECP at three different levels (60, 80, and 600 μg) to dorsal skin for six days. Skin lesion severity, skin color, skin barrier function (SBF, as indicated by water content and water-holding capacity (WHC)), histopathological abnormalities, cytokine levels, filaggrin and Intercellular Adhesion Molecule-1 (ICAM-1) expression, and phosphorylation of MAPK (Mitogen-Activated Protein Kinase) signaling molecules were assessed. EECP treatment significantly alleviated the CD-associated dermal symptoms induced by DNFB, including skin fissures, scabbing, roughness, changes in color, water content, and WHC, as well as petechiae. EECP also prevented histopathological abnormalities such as epidermal hyperplasia, spongiotic changes, and immune cell infiltration. In addition, EECP suppressed the production of pro-inflammatory cytokines, viz. TNF-α, IFN-γ, IL-6, and MCP-1. In addition, EECP restored filaggrin expression and inhibited ERK (Extracellular signal-regulated kinases) phosphorylation and ICAM-1 expression in HaCaT cells. In summary, C. papaya peel demonstrated therapeutic potential by effectively suppressing inflammation and restoring SBF. These findings support the potential use of EECP as a safe and effective botanical candidate for the treatment of CD and the promotion of overall skin health Full article

(This article belongs to the Special Issue Molecular Mechanisms and Therapeutic Targeting of Inflammatory Complications)

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19 pages, 4109 KB

Open AccessArticle

Modulation of AMPK/NLRP3 Signaling Mitigates Radiation-Induced Lung Inflammation by a Synthetic Lipoxin A4 Analogue

by Sun Ho Min, Jae-Ho Shin, Sunjoo Park, Ronglan Cui, Youn Ji Hur, Woo Hyun Jeong, Sang Yeon Kim, Younghwa Na and Jaeho Cho

Int. J. Mol. Sci. 2025, 26(22), 10832; https://doi.org/10.3390/ijms262210832 - 7 Nov 2025

Viewed by 493

Abstract

Radiation-induced lung inflammation (RILI) is a major complication of thoracic radiotherapy, characterized by excessive inflammation and subsequent fibrosis that compromise pulmonary function and treatment outcomes. This study explores the pharmacological properties of a newly synthesized Lipoxin A4 analogue (CYNC-2) to mitigate RILI by modulating the AMP-activated protein kinase (AMPK)/NOD-like receptor family pyrin domain containing 3(NLRP3) inflammasome pathway. A murine RILI model was established in mice by delivering a single high-dose (ablative) X-ray irradiation to the left lung. Mice in the treatment group received CYNC-2 via tail-vein injection three times per week for 2 weeks. The effects of CYNC-2 on RILI were evaluated histological, immunohistochemical analysis of lung tissues, cytokine profiling, lung function testing using a FlexiVent system, and micro-computed tomography (micro-CT) imaging of lung damage. In parallel, two human lung cell lines—L132 (normal bronchial epithelial cells) and A549 (lung carcinoma cells)—were irradiated with 6 Gy X-rays and treated with CYNC-2 to assess cell viability and changes in AMPK/NLRP3 pathway markers via qPCR and immunofluorescence. Lung tissue sample from patients who underwent thoracic radiotherapy were also examined to validate key findings. CYNC-2 activated AMPK and inhibited mTOR signaling, which suppressed NLRP3 inflammasome activation and led to reduced secretion of pro-inflammatory cytokines (IL-1β, IL-6, and TGF-β1). In vitro, CYNC-2 mitigated radiation-induced inflammatory responses and preserved cellular viability. Overall, CYNC-2 effectively dampened acute pulmonary in the RILI model. These findings suggest that targeting the AMPK/NLRP3 inflammasome pathway via a stable LXA4 analogue such as CYNC-2 is a promising therapeutic strategy to improve clinical outcomes for patients receiving thoracic radiation therapy. Full article

(This article belongs to the Special Issue Molecular Mechanisms and Therapeutic Targeting of Inflammatory Complications)

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26 pages, 2317 KB

Open AccessArticle

Dendritic Polyglycerol Sulfate Reduces Inflammation Through Inhibition of the HMGB1/RAGE Axis in RAW 264.7 Macrophages

by Marten Kagelmacher, Cristina S. Quella, Emma Kautz, Anna Klumpp, Felix Weichert, Issan Zhang, Dusica Maysinger, Poornima G. Wedamulla, Suzana K. Straus, Thomas Risse, Rainer Haag, Marina Pigaleva and Jens Dernedde

Int. J. Mol. Sci. 2025, 26(21), 10440; https://doi.org/10.3390/ijms262110440 - 27 Oct 2025

Viewed by 662

Abstract

High Mobility Group Box 1 (HMGB1) is a central pro-inflammatory mediator released from damaged or stressed cells, where it activates receptors such as the Receptor for Advanced Glycation Endproducts (RAGE). Dendritic polyglycerol sulfate (dPGS), a hyperbranched polyanionic polymer, is known for its anti-inflammatory activity. In this study, we examined how dPGS modulates HMGB1-driven signaling in RAW 264.7 macrophages and human microglia. Recombinant human HMGB1 expressed in Escherichia coli (E. coli) was purified by nickel-nitrilotriacetic acid (Ni-NTA) and heparin chromatography. Proximity ligation assays (PLA) revealed that dPGS significantly disrupted HMGB1/RAGE interactions, particularly under lipopolysaccharide (LPS) stimulation, thereby reducing inflammatory signaling complex formation. This correlated with reduced activation of the nuclear factor kappa B (NF-κB) pathway, demonstrated by decreased nuclear translocation and transcriptional activity. Reverse transcription polymerase chain reaction (RT-PCR) and quantitative real-time PCR (RT-qPCR) showed that dPGS suppressed HMGB1- and LPS-induced transcription of tumor necrosis factor alpha (TNF-α), interleukin-6 (IL-6), monocyte chemoattractant protein-1 (MCP-1), cyclooxygenase-2 (COX-2), and inducible nitric oxide synthase (iNOS). Enzyme-linked immunosorbent assay (ELISA) and Griess assays confirmed reduced TNF-α secretion and nitric oxide production. Electron paramagnetic resonance (EPR) spectroscopy further showed that dPGS altered HMGB1/soluble RAGE (sRAGE) complex dynamics, providing mechanistic insight into its receptor-disruptive action. Full article

(This article belongs to the Special Issue Molecular Mechanisms and Therapeutic Targeting of Inflammatory Complications)

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14 pages, 683 KB

Open AccessArticle

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 - 24 Oct 2025

Viewed by 450

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, 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)

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Review

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21 pages, 3052 KB

Open AccessReview

Salivary Biomarkers in Crohn’s Disease and Ulcerative Colitis: A Scoping Review and Evidence Map

by Karina Oliveira Santos, Ligia Yukie Sassaki, Maiara Brusco De Freitas, Julio Pinheiro Baima, Murilo Henrique Faria, Anna Luisa Bizotto, Júlia Pardini Benício and Ana Carolina Magalhães

Int. J. Mol. Sci. 2025, 26(22), 11195; https://doi.org/10.3390/ijms262211195 - 19 Nov 2025

Viewed by 578

Abstract

Salivary biomarkers have been explored as potential non-invasive tools for the diagnosis and monitoring of inflammatory bowel diseases (IBD), including Crohn’s Disease (CD) and Ulcerative Colitis (UC). This study presents a scoping review and evidence mapping on the use of saliva as a matrix in which biomarkers can be identified for these conditions. A systematic search of multiple databases and studies was conducted until 28 January 2025, resulting in the selection of 12 relevant articles. The quantified evidence synthesis identified eight molecular and microbial categories. Of these, four classes, including cytokines, microRNAs, calprotectin, and the microbiome, have demonstrated the most consistent potential. Alterations in these biomarkers, such as an increase in the Prevotella genus within the microbiome, and elevated PSMA7 levels, may reflect disruptions in intestinal barrier integrity and immune response. However, factors such as oral health status, hygiene habits, and medication must be carefully considered. Therefore, further clinical research is essential to validate specific biomarkers. Full article

(This article belongs to the Special Issue Molecular Mechanisms and Therapeutic Targeting of Inflammatory Complications)

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24 pages, 2700 KB

Open AccessReview

Oxylipins in Atherosclerosis: Their Role in Inflammation, Diagnosis, and Therapeutic Perspectives

by Dmitry V. Chistyakov, Vasiliy V. Chistyakov and Marina G. Sergeeva

Int. J. Mol. Sci. 2025, 26(21), 10577; https://doi.org/10.3390/ijms262110577 - 30 Oct 2025

Viewed by 657

Abstract

Atherosclerosis, the principal pathology underlying cardiovascular diseases, is now recognized as a chronic inflammatory disorder of the arterial wall. This review focuses on the central role of oxylipins, a diverse family of bioactive lipids derived from polyunsaturated fatty acids (PUFAs), in the inflammatory processes driving atherosclerosis. We synthesize evidence that oxylipins produced via cyclooxygenase (COX), lipoxygenase (LOX), cytochrome P450 (CYP), anandamide (AEA) pathways and non-enzymatic transformations of PUFAs are pivotal modulators of vascular function, immune cell recruitment, and plaque stability. The balance between pro-inflammatory mediators and specialized pro-resolving mediators (SPMs) is critical; a shift towards inflammation underlies disease progression. Advances in lipidomics now enable comprehensive oxylipin profiling, revealing distinct signatures with significant diagnostic and prognostic potential for assessing coronary artery disease severity and predicting future cardiovascular events. Therapeutically, while current anti-inflammatory strategies target downstream pathways, this review highlights emerging approaches that modulate the oxylipin system directly. These include promoting SPMs synthesis through omega-3 supplementation, inhibiting pro-inflammatory leukotriene production, and preserving cardioprotective epoxyeicosatrienoic acids (EETs) via soluble epoxide hydrolase (sEH) inhibition. A deeper understanding of these complex oxylipin networks promises to yield novel biomarkers and targeted therapies designed to restore inflammatory homeostasis and combat atherosclerotic cardiovascular disease. Full article

(This article belongs to the Special Issue Molecular Mechanisms and Therapeutic Targeting of Inflammatory Complications)

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21 pages, 1260 KB

Open AccessReview

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 - 24 Oct 2025

Viewed by 4381

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 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

Open AccessReview

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

Cited by 1 | Viewed by 8539

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 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

Open AccessReview

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

Cited by 4 | Viewed by 4561

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 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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