Inflammation—The Surprising Bridge between Diseases

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: 15 August 2025 | Viewed by 1619

Special Issue Editors


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Guest Editor
Department of Pathophysiology, “Grigore T. Popa” University of Medicine and Pharmacy, 16 Universitatii Street, 700115 Iasi, Romania
Interests: cardiovascular diseases; metabolic diseases; diabetes mellitus; antioxidants
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E-Mail Website
Guest Editor

E-Mail Website
Guest Editor
Department of Pathophysiology, “Grigore T. Popa” University of Medicine and Pharmacy, 16 Universitatii Street, 700115 Iasi, Romania
Interests: cardiovascular diseases; hypercoagulability; acute cardiac care; noninvasive cardiovascular imaging techniques
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The inflammatory response is part of our biology and is the physiological mechanism of defense against viral, bacterial, fungal and parasite aggression. However, under the pressure of a wide spectrum of stressors, this mechanism turns against us.

Low-grade inflammation is a chronic imbalanced response that perpetuates metabolic disruption and tissue destruction. It contributes to the impairment of lung function, mainly by affecting the peripheral airways and parenchyma. It characterizes adipose tissue dysfunction and insulin resistance in obesity and diabetes. Together with the accelerated foam cell formation it triggers, it paves the pathway for atherosclerosis, and further, for ischemic heart disease and peripheral artery disease. It induces the accelerated deterioration of the bioprosthetic valves. It is responsible for structural and functional changes in the gastrointestinal tract and liver, leading to inflammatory bowel disease and fatty liver disease. It is a major contributor to joint destruction in rheumatoid arthritis. It favors the initiation, growth, progression and metastasis of cancer.

In this context, we consider of great interest the precise characterization of the molecular pathways that lead to the clinically manifest disease. The identification of organ-specific biomarkers of low-grade inflammation would allow for the early identification of imbalance and therapeutic intervention before the onset of irreversible damage. The monitoring of treatment response would be greatly improved by the existence of biomarkers that would signal early the recurrence of the imbalance.

We must come to the aid of clinicians from different specialties who strive to treat specific organ damage and identify the stages of the pathogenic cascade amenable to therapeutic intervention, as well as making efforts to implement the found solutions in practice. Targeting the earliest possible stages in the pathogenic cascade is a priority.

We invite you contribute to this Special Issue and share your experience in this field. Both original studies and reviews are welcome for submission. Only together will we be able to provide robust guidelines for a targeted approach to the pathogenic links of inflammation and stop the destructive spiral of organ damage.

Prof. Dr. Manuela Ciocoiu
Dr. Minerva Codruta Badescu
Dr. Iris Bararu-Bojan
Guest Editors

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Keywords

  • low-grade inflammation
  • lung inflammation
  • atherosclerosis
  • ischemic heart disease
  • peripheral artery disease
  • inflammatory bowel disease
  • fatty liver disease
  • inflammatory rheumatic diseases
  • cancer

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Published Papers (1 paper)

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Research

19 pages, 3859 KiB  
Article
Anti-Inflammatory and Anti-Migratory Effects of Morin on Non-Small-Cell Lung Cancer Metastasis via Inhibition of NLRP3/MAPK Signaling Pathway
by Punnida Arjsri, Kamonwan Srisawad, Sonthaya Umsumarng, Pilaiporn Thippraphan, Songyot Anuchapreeda and Pornngarm Dejkriengkraikul
Biomolecules 2025, 15(1), 103; https://doi.org/10.3390/biom15010103 - 10 Jan 2025
Viewed by 1186
Abstract
Non-small-cell lung cancer (NSCLC) remains the leading cause of cancer-related deaths globally, with a persistently low five-year survival rate of only 14–17%. High rates of metastasis contribute significantly to the poor prognosis of NSCLC, in which inflammation plays an important role by enhancing [...] Read more.
Non-small-cell lung cancer (NSCLC) remains the leading cause of cancer-related deaths globally, with a persistently low five-year survival rate of only 14–17%. High rates of metastasis contribute significantly to the poor prognosis of NSCLC, in which inflammation plays an important role by enhancing tumor growth, angiogenesis, and metastasis. Targeting inflammatory pathways within cancer cells may thus represent a promising strategy for inhibiting NSCLC metastasis. This study evaluated the anti-inflammatory and anti-metastatic properties of morin, a bioactive compound derived from a Thai medicinal herb, focusing on its effects on NLRP3 inflammasome-mediated pathways in an in vitro NSCLC model. The A549 and H1299 cell lines were stimulated with lipopolysaccharide (LPS) and adenosine triphosphate (ATP) to activate the NLRP3 pathway. The inhibition effects exhibited by morin in reducing pro-inflammatory secretion in LPS- and ATP-stimulated NSCLC cells were assessed by ELISA, while wound healing and trans-well invasion assays evaluated its impact on cell migration and invasion. RT-qPCR measurement quantified the expression of inflammatory genes, and zymography and Western blotting were used to examine changes in invasive protein levels, epithelial-to-mesenchymal transition (EMT) markers, and underlying molecular mechanisms. Our findings demonstrated the significant ability of morin to decrease the production of IL-1β, IL-18, and IL-6 in a dose-dependent manner (p < 0.05), as well as suppress NSCLC cell migration and invasion. Morin downregulated invasive proteins (MMP-2, MMP-9, u-PAR, u-PA, MT1-MMP) and EMT markers (fibronectin, N-cadherin, vimentin) (p < 0.01) while also reducing the mRNA levels of NLRP3, IL-1β, IL-18, and IL-6. Mechanistic investigations revealed that morin suppressed NLRP3 inflammasome activity and inactivated MAPK pathways. Specifically, it decreased the expression of NLRP3 and ASC proteins and reduced caspase-1 activity, while reducing the phosphorylation of ERK, JNK, and p38 proteins. Collectively, these findings suggest that morin’s inactivation of the NLRP3 inflammasome pathway could offer a novel therapeutic strategy for counteracting pro-tumorigenic inflammation and metastatic progression in NSCLC. Full article
(This article belongs to the Special Issue Inflammation—The Surprising Bridge between Diseases)
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