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Molecular Mechanisms and Innovative Therapeutic Approaches in Inflammatory Diseases, Pioneering Precision Medicine Solutions

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A special issue of Current Issues in Molecular Biology (ISSN 1467-3045). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: 15 May 2025 | Viewed by 4871

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Special Issue Editors

Dr. Hector A. Cabrera-Fuentes

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UNAM-UABJO Research Center, Universidad Autónoma Benito Juárez de Oaxaca, Oaxaca 68120, Mexico
Interests: basic science and clinical research in organ protection against acute ischaemia/reperfudion injury with a special focus on cardiac protection and acute inflammation and remodeling; basic science and translational research in atherosclerosis and chronic inflammation processes

Prof. Dr. Klaus T. Preissner

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Department of Cardiology, Kerckhoff-Heart Research Institute, Faculty of Medicine, Justus-Liebig-University, 35392 Giessen, Germany
Interests: innate immune processes in host-pathogen interactions; inflammation; wound healing; thrombosis; cardiovascular diseases; lung disease

Prof. Dr. Elisabeth Deindl

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Walter-Brendel-Centre of Experimental Medicine, University Hospital, Ludwig-Maximilians-Universität München, 81377 Munich, Germany
Interests: cardiovascular research; immunology
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Special Issue Information

Dear Colleagues,

Inflammatory diseases, ranging from autoimmune disorders to chronic inflammatory conditions, pose significant challenges to global health. The complexity of inflammation involves intricate molecular pathways, including immune system dysregulation, cytokine signaling, and oxidative stress, which vary among individuals and disease states. Advances in molecular biology and precision medicine are unlocking new insights into these mechanisms, offering the potential for highly targeted and effective therapies. This Special Issue aims to delve into the molecular mechanisms that drive inflammatory diseases, with a focus on identifying novel therapeutic targets and pathways. By exploring innovative therapeutic approaches—such as biologics, small molecules, gene therapies, and personalized treatment regimens—this Special Issue will shed light on the future of inflammation treatment through precision medicine. We invite submissions that provide groundbreaking research, clinical studies, and reviews on molecular drivers of inflammation, disease biomarkers, and personalized therapeutic strategies that hold the potential to transform patient outcomes in inflammatory diseases.

Dr. Hector A. Cabrera-Fuentes
Prof. Dr. Klaus T. Preissner
Prof. Dr. Elisabeth Deindl
Guest Editors

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Keywords

inflammatory diseases
autoimmune disorders
cytokine signaling
oxidative stress
therapies

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Published Papers (8 papers)

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Research

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11 pages, 1066 KiB

Open AccessArticle

Effects of Caffeine on THP-1 Myelogenous Cell Inflammatory Gene Expression

by Zeyar T. Htun, Thomas M. Raffay, Richard J. Martin, Peter M. MacFarlane and Tracey L. Bonfield

Curr. Issues Mol. Biol. 2025, 47(4), 248; https://doi.org/10.3390/cimb47040248 - 2 Apr 2025

Viewed by 308

Abstract

Caffeine is administered to preterm infants in neonatal intensive care units for prevention and treatment of apnea of prematurity. Although caffeine’s primary effect is to impact the respiratory drive of preterm infants, caffeine also has anti-inflammatory properties. This study investigated the role of caffeine on the inflammatory gene expression in THP-1 pre-monocytes exposed to lipopolysaccharide (LPS) in vitro, mimicking a clinical pro-inflammatory scenario. The effects of different physiologic dosages of caffeine administration post-LPS (treatment with caffeine) and pre-LPS (prophylaxis with caffeine) on pro-inflammatory gene expressions (TNF-α, NF-κB, IL-8, PPARγ) of the THP-1 cells were investigated. The post-LPS group showed a dose-dependent decrease in TNF-α at a caffeine concentration of 100 μM and NF-κB gene expression at 50 and 100 μM, with the implication that this is an optimal anti-inflammatory caffeine concentration range. Clinically, this would correspond to a serum caffeine level between 10 and 20 μg/mL, respectively. For the pre-LPS group, TNF-α and NF-κB gene expression decreased at all studied caffeine concentrations. These findings point to caffeine’s potential therapeutic capacity in regulating monocyte inflammatory responses to gram-negative infections in addition to regulating neuron response in the brainstem for preterm infants. Full article

(This article belongs to the Special Issue Molecular Mechanisms and Innovative Therapeutic Approaches in Inflammatory Diseases, Pioneering Precision Medicine Solutions)

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15 pages, 2754 KiB

Open AccessArticle

Synergistic Anti-Inflammatory Effects of Pomegranate Peel–Hawthorn Combinations in Ulcerative Colitis: Network Pharmacology Prediction and Experimental Validation

by Shouqing Zhang, Quanyuan Qiu, Mengzhen Yuan, Jiajia Yu, Weiwei Gao, Xi Wang, Zhen Liu, Peng Yu, Cen Xiang and Yuou Teng

Curr. Issues Mol. Biol. 2025, 47(4), 243; https://doi.org/10.3390/cimb47040243 - 1 Apr 2025

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Abstract

Ulcerative colitis (UC) is a chronic inflammatory bowel disease characterized by complex pathogenesis involving dysregulated immunity and gut microbiota imbalance, demanding innovative therapeutic strategies. This study investigates the synergistic therapeutic potential of pomegranate peel–hawthorn combinations and their active constituents (ellagic acid and maslinic acid) through an integrative approach combining network pharmacology, in vitro/in vivo experiments, and gut microbiota analysis. Network pharmacology identified 61 shared therapeutic targets (p < 0.05 for pathway enrichment) and revealed complementary mechanisms: pomegranate peel primarily modulated AGE-RAGE/PI3K-Akt pathways, while hawthorn targeted IL-17/NF-κB signaling. Experimental validation demonstrated potent synergistic anti-inflammatory effects (combination index < 1), with optimal combinations reducing nitric oxide production by 52.35% (herbal extracts, p < 0.05) and 74.4% (active monomers, p < 0.05). In DSS-induced UC mice, combinatorial therapies significantly suppressed pro-inflammatory cytokines (TNF-α: 204.78 vs. 446.52 pg/mL in UC group, p < 0.05; IL-6: 33.19 vs. 64.86 pg/mL, p < 0.05), restored colonic SOD activity (72.31 vs. 50.10 U/mg·prot in UC group, p < 0.01), and alleviated histopathological damage, outperforming monotherapeutics. Gut microbiota analysis revealed the recovery of α-diversity indices and normalized Bacteroidota/Bacillota ratios. Mechanistically, the combinations suppressed MAPK/NF-κB signaling cascades, reducing p-p38/p38 (p < 0.01 vs. UC group) and p-ERK1/2/ERK1/2 (p < 0.01 vs. UC group) phosphorylation. These findings establish that pomegranate peel–hawthorn formulations exert multi-modal therapeutic effects through the synergistic inhibition of pathways, mitigation of oxidative stress, and restoration of the microbiota, offering a scientifically validated approach for UC management rooted in traditional medicine principles. Full article

(This article belongs to the Special Issue Molecular Mechanisms and Innovative Therapeutic Approaches in Inflammatory Diseases, Pioneering Precision Medicine Solutions)

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18 pages, 3306 KiB

Open AccessArticle

Hepatic Growth Factor as a Potential Biomarker for Lung Adenocarcinoma: A Multimodal Study

by Mengxuan Sun, Yang Yu, Hanci Zhu, Yan Yao, Xintong Zhou, Xue Wang, Yubao Zhang, Xiaowei Xu, Jing Zhuang and Changgang Sun

Curr. Issues Mol. Biol. 2025, 47(3), 208; https://doi.org/10.3390/cimb47030208 - 19 Mar 2025

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Abstract

(1) Background: Despite previous studies linking inflammatory cytokines to lung adenocarcinoma (LUAD), their causal mechanisms remain unclear. This study aims to explore the causal relationship between inflammatory cytokines and LUAD to fill this knowledge gap. (2) Methods: This study employs a comprehensive approach, integrating Mendelian randomization (MR) analysis, single-cell RNA sequencing (scRNA-seq), and transcriptomic sequencing (RNA-seq) data to investigate the relationship between inflammatory cytokines and LUAD. (3) Results: In forward MR analysis, elevated levels of hepatocyte growth factor (HGF), interleukin-1 receptor antagonist (IL-1RA), IL-5, monocyte chemoattractant protein-3, and monokine induced by interferon-γ were causally associated with an increased risk of LUAD. In reverse MR analysis, LUAD exhibited a positive causal relationship with the levels of regulated upon activation normal T cell expressed and secreted factor (RANTES) and stromal cell-derived factor-1α. The scRNA-seq data further identified specific cell populations that may influence LUAD onset and progression through the expression of particular inflammatory genes and intercellular communication. RNA-seq data analysis highlighted the role of the HGF gene in LUAD diagnosis, demonstrating its strong correlation with patient prognosis and immune cell infiltration within the tumor microenvironment. (4) Conclusions: The findings reveal a causal relationship between inflammatory cytokines and LUAD, with HGF emerging as a potential biomarker of significant clinical relevance. This study provides new insights into the molecular mechanisms underlying LUAD and lays the foundation for future therapeutic strategies. Full article

(This article belongs to the Special Issue Molecular Mechanisms and Innovative Therapeutic Approaches in Inflammatory Diseases, Pioneering Precision Medicine Solutions)

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14 pages, 1938 KiB

Open AccessArticle

Urinary Kim-1 Correlates with Interstitial Nephritis Activity in Patients with Microscopic Polyangiitis

by Chisato Ashida, Yuji Nozaki, Jinhai Li, Hiroki Akazawa, Kazuya Kishimoto, Koji Kinoshita and Itaru Matsumura

Curr. Issues Mol. Biol. 2025, 47(3), 196; https://doi.org/10.3390/cimb47030196 - 16 Mar 2025

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Abstract

Background: Microscopic polyangiitis (MPA) is a type of necrotizing vasculitis that primarily affects small vessels and belongs to the spectrum of anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitides (AAVs). While previous studies have identified potential prognostic biomarkers, further research is needed to validate a reliable marker for risk stratification in clinical practice. Kidney injury molecule-1 (Kim-1), a transmembrane protein expressed on proximal tubular epithelial cells, has been implicated in tubular damage. This study investigated the potential of Kim-1 as a biomarker in MPA. Methods: Kidney biopsy tissues, along with urine and blood samples, were retrospectively analyzed from 52 MPA patients and compared to urine samples from 7 healthy controls. Global disease activity was assessed using the Birmingham vasculitis activity score (BVAS) and vasculitis damage index, while renal disease activity was evaluated using renal BVAS (BVAS-R). Results: Urinary Kim-1 levels were significantly elevated in MPA patients compared to healthy controls. Urinary Kim-1 was positively correlated with the Mayo Clinic Chronicity Score (MCCS) but not with the ANCA Kidney Risk Score (AKRiS), whereas tubular Kim-1 was associated with AKRiS but not with MCCS, indicating their distinct pathological significance. Higher tubular Kim-1 expression was observed in patients with elevated BVAS-R. Urinary Kim-1 levels correlated with proteinuria and were associated with the Mayo Clinic Chronicity Score (MCCS) and ANCA Kidney Risk Score (AKRiS) but not with glomerular lesion severity. Unlike C-reactive protein (CRP), neither urinary nor tubular Kim-1 predicted MPA recurrence. Conclusions: Urinary Kim-1 reflects histopathologic findings and renal impairment but does not predict systemic disease activity or recurrence in MPA, demonstrating its potential clinical utility as a biomarker for assessing chronic renal damage. Full article

(This article belongs to the Special Issue Molecular Mechanisms and Innovative Therapeutic Approaches in Inflammatory Diseases, Pioneering Precision Medicine Solutions)

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11 pages, 1582 KiB

Open AccessArticle

A Pilot Study on the Role of TRAFs in the Development of SARS-CoV-2 Infection Before and After Immunization with AstraZeneca Chadox1 in Mice

by Mounia Ammara, Inass Samiry, Younes Zaid, Mounia Oudghiri and Abdallah Naya

Curr. Issues Mol. Biol. 2025, 47(3), 165; https://doi.org/10.3390/cimb47030165 - 28 Feb 2025

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Abstract

The TRAF family of molecules are intracellular signaling adaptors that regulate various signaling pathways. These pathways are not only mediated by the TNFR superfamily and the Toll-like receptor/IL-1 receptor superfamily but also by unconventional cytokine receptors like IL-6 and IL-17 receptors. Overactive immune responses caused by TRAF signaling following the activation of these receptors frequently result in inflammatory and autoimmune diseases such as rheumatoid arthritis, inflammatory bowel disease, psoriasis, and autoinflammatory syndromes. Therefore, it is crucial to comprehend the signaling processes controlled by TRAFs, which have a significant influence on the determination of cell fate (life or death) and the functioning, specialization, and endurance of cells in the innate and adaptive immune systems. Our data indicate that the dysregulation of cellular expression and/or signaling of TRAFs leads to the excessive production of pro-inflammatory cytokines, hence promoting abnormal activation of immune cells. The objective of our investigation was to comprehend the function of these molecules in SARS-CoV-2 infection both prior to and during SARS-CoV-2 vaccination. Our results demonstrate a clear inactivation of the TRAF5 and TRAF6 genes when infection occurs after immunization, in contrast to infection without prior vaccination. This can bolster the belief that immunization is essential while also demonstrating the involvement of these molecules in the pathogenesis of SARS-CoV-2. Full article

(This article belongs to the Special Issue Molecular Mechanisms and Innovative Therapeutic Approaches in Inflammatory Diseases, Pioneering Precision Medicine Solutions)

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12 pages, 2465 KiB

Open AccessArticle

Tumor Necrosis Factor Superfamily 14 Regulates the Inflammatory Response of Human Dental Pulp Stem Cells

by Abdulelah Alrshedan, Mona Elsafadi, Manikandan Muthurangan and Solaiman Al-Hadlaq

Curr. Issues Mol. Biol. 2024, 46(12), 13979-13990; https://doi.org/10.3390/cimb46120836 - 11 Dec 2024

Viewed by 1082

Abstract

Dental caries is a highly prevalent chronic disease that leads to dental pulp inflammation. It is treated by removing the damaged tooth structure and applying a material that promotes resolution of pulpal inflammation. Tumor necrosis factor superfamily 14 (TNFSF14) is an immunomodulatory cytokine and a member of the TNF superfamily. This study aimed to evaluate the effect of TNFSF14 on the levels of inflammatory cytokines involved in pulpal inflammation using lipoteichoic acid (LTA)-induced human dental pulp stem cells (hDPSCs). hDPSCs were cultured and induced with LTA, followed by treatment with TNFSF14 at 25 and 50 ng/mL. Cellular viability was evaluated using the Alamar Blue assay. The levels of inflammatory cytokines IL-6, IL-8, IL-10, and TNF-α were quantified using reverse transcription–quantitative polymerase chain reaction (RT–qPCR) and enzyme-linked immunosorbent assay (ELISA). TNFSF14 at 25 and 50 ng/mL significantly reduced the mRNA and protein levels of pro-inflammatory cytokines TNF-α, IL-6, and IL-8, and increased the anti-inflammatory cytokine IL-10. In addition, TNFSF14-treated groups enhanced cell viability. Adding TNFSF14 to LTA-induced hDPSCs regulated the production of inflammatory cytokines by lowering the levels of IL-6, IL-8, and TNF-α and elevating IL-10 levels. Full article

(This article belongs to the Special Issue Molecular Mechanisms and Innovative Therapeutic Approaches in Inflammatory Diseases, Pioneering Precision Medicine Solutions)

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Review

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28 pages, 2105 KiB

Open AccessReview

DNA Methylation in Ph-Negative Myeloproliferative Neoplasms: Prognostic Role and Therapeutic Implications

by Paola Barone, Adele Bottaro, Rossana Leanza, Fabio Stagno and Alessandro Allegra

Curr. Issues Mol. Biol. 2025, 47(4), 227; https://doi.org/10.3390/cimb47040227 - 26 Mar 2025

Viewed by 172

Abstract

Myeloproliferative neoplasms are clonal hematological neoplasms characterized by excessive proliferation of cells of erythroid, granulocytic, and megakaryocytic lineage. The genetic mechanisms underlying this group of blood diseases are now known, but new perspectives have recently emerged in the field of epigenetics and particularly related to the possible role of DNA methylation in disease development and progression. DNA methylation regulates different cellular processes, such as proliferation, differentiation, and apoptosis. In myeloproliferative neoplasms, a link has been found between abnormal methylation patterns, such as hypermethylation of tumor suppressors or, conversely, oncogenes hypomethylation, with the progression of the disease, spreading important prognostic and therapeutic implications. This review aims to investigate the relationship between methylation alterations and myeloproliferative neoplasms, emphasizing the ways by which epigenetic dysregulation promotes disease biology. Full article

(This article belongs to the Special Issue Molecular Mechanisms and Innovative Therapeutic Approaches in Inflammatory Diseases, Pioneering Precision Medicine Solutions)

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20 pages, 1291 KiB

Open AccessReview

Epigenetic Mechanisms in CRSwNP: The Role of MicroRNAs as Potential Biomarkers and Therapeutic Targets

by Alkmini Gatsounia, Georgios Schinas, Gerasimos Danielides, Katerina Grafanaki, Nicholas Mastronikolis, Constantinos Stathopoulos and Spyridon Lygeros

Curr. Issues Mol. Biol. 2025, 47(2), 114; https://doi.org/10.3390/cimb47020114 - 10 Feb 2025

Cited by 1 | Viewed by 952

Abstract

Chronic rhinosinusitis with nasal polyps (CRSwNP) is a prevalent inflammatory disease of the upper airway, contributing significantly to the global disease burden. CRSwNP is characterized by sustained and exaggerated inflammation, accompanied by marked changes in gene and protein expression regulated through intricate molecular mechanisms. MicroRNAs (miRNAs), small single-stranded RNA molecules that regulate gene expression at transcriptional and post-transcriptional levels, have emerged as pivotal players in CRSwNP pathophysiology. Dysregulated miRNA expression is implicated in numerous human diseases, including cancer, asthma, and inflammatory disorders, highlighting their broad clinical relevance. In CRSwNP, miRNAs influence important inflammatory pathways, including T2 immune responses and epithelial–mesenchymal transition (EMT), which leads to chronic inflammation and tissue remodeling. Profiling studies have identified specific miRNAs as potential biomarkers for disease severity, prognosis, and therapeutic response, offering a pathway to personalized medicine. Furthermore, advances in small extracellular vesicles (sEVs) and exosomes, which naturally transport miRNAs, provide innovative avenues for targeted miRNA delivery, minimizing systemic side effects. This review explores current knowledge on miRNA expression and function in CRSwNP, emphasizing their role in disease pathogenesis and their potential as biomarkers and therapeutic targets. Full article

(This article belongs to the Special Issue Molecular Mechanisms and Innovative Therapeutic Approaches in Inflammatory Diseases, Pioneering Precision Medicine Solutions)

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