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New Molecular Mechanisms and Markers in Inflammatory Disorders, 3rd Edition
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New Molecular Mechanisms and Markers in Inflammatory Disorders, 3rd Edition

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Immunology".

Deadline for manuscript submissions: 20 May 2025 | Viewed by 2465

Special Issue Editor

Dr. Elena Vianello

E-Mail Website
Guest Editor
Department of Biomedical Sciences for Health, Università degli Studi di Milano, Milan, Italy
Interests: inflammation; inflammatory disorders; biomarkers; molecular mechanism of inflammation; molecular signaling
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Inflammation participates in hosts’ defences against infectious agents and injury, but it also contributes to the pathophysiology of many chronic diseases, ranging from cancer to biomechanical injuries and from chronic to acute disorders. For this reason, the discovery of new, inflammation-linked biomarkers is the goal of many studies focused on the pathogenesis, the diagnosis, the prognosis, and the therapeutical approaches of inflammation-associated comorbidities. The intent of this Special Issue is to present research papers and reviews focused on new biomarkers of inflammation-associated disorders, which highlight their molecular mechanisms during the onset and progression of pathological states such as cancer, immune diseases, cardiovascular-associated disorders, metabolic diseases, and all other pathological states linked to inflammation. This knowledge should facilitate the development of novel strategies to predict disease susceptibility, target and monitor therapies, and ultimately, develop new approaches to the prevention and treatment of diseases associated with inflammation.

Dr. Elena Vianello
Guest Editors

Manuscript Submission Information

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Keywords

  • inflammation
  • inflammatory disorders
  • biomarkers
  • molecular mechanism of inflammation
  • molecular signaling

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Published Papers (4 papers)

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Review

26 pages, 1106 KiB  
Review
The Advanced Glycation End-Products (AGE)–Receptor for AGE System (RAGE): An Inflammatory Pathway Linking Obesity and Cardiovascular Diseases
by Elena Vianello, Antonio P. Beltrami, Aneta Aleksova, Milijana Janjusevic, Alessandra L. Fluca, Massimiliano M. Corsi Romanelli, Lucia La Sala and Elena Dozio
Int. J. Mol. Sci. 2025, 26(8), 3707; https://doi.org/10.3390/ijms26083707 - 14 Apr 2025
Viewed by 426
Abstract
The AGE (advanced glycation end-products)–RAGE (receptor for AGE) system is a pro-inflammatory pathway that contributes to the pathogenesis of obesity and obesity-related cardiovascular disorders (CVD). Circulating AGE and the soluble form of RAGE (sRAGE) has been suggested as a potential biomarker of CVD [...] Read more.
The AGE (advanced glycation end-products)–RAGE (receptor for AGE) system is a pro-inflammatory pathway that contributes to the pathogenesis of obesity and obesity-related cardiovascular disorders (CVD). Circulating AGE and the soluble form of RAGE (sRAGE) has been suggested as a potential biomarker of CVD related to obesity. In this study, we aim to (1) summarize the current knowledge about the role of obesity in the onset and progression of CVD, (2) discuss the role of the AGE–RAGE system as a pathway promoting obesity and linking obesity to CVD, and (3) highlight available strategies for reducing AGE–RAGE system activation and the associated beneficial effects. Full article
(This article belongs to the Special Issue New Molecular Mechanisms and Markers in Inflammatory Disorders, 3rd Edition)
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Graphical abstract

14 pages, 1130 KiB  
Review
Cardio-Rheumatic Diseases: Inflammasomes Behaving Badly
by Farah Issa, Marah Abdulla, Faizah D. Retnowati, Huda Al-Khawaga, Hanin Alhiraky, Khalid M. Al-Harbi, Amal Al-Haidose, Zaid H. Maayah and Atiyeh M. Abdallah
Int. J. Mol. Sci. 2025, 26(8), 3520; https://doi.org/10.3390/ijms26083520 - 9 Apr 2025
Viewed by 223
Abstract
Cardio-rheumatology is an evolving and interdisciplinary field lying at the intersection of rheumatology and cardiovascular medicine that recognizes that individuals with autoimmune and inflammatory rheumatic complications have a much higher likelihood of developing cardiovascular diseases (CVDs). Inflammasomes are multiprotein complexes stimulated by the [...] Read more.
Cardio-rheumatology is an evolving and interdisciplinary field lying at the intersection of rheumatology and cardiovascular medicine that recognizes that individuals with autoimmune and inflammatory rheumatic complications have a much higher likelihood of developing cardiovascular diseases (CVDs). Inflammasomes are multiprotein complexes stimulated by the immune system after the detection of pathogens or cellular injury. Inflammasomes undergo a two-stage activation process initiated by nuclear factor (NF)-κB, subsequently playing a crucial role in innate immunity through activation of caspase 1 and the consequent release of proinflammatory cytokines such as IL-18 and IL-1β. However, a loss of control of inflammasome activation can cause inflammatory diseases in humans. Recent studies have focused on the role of inflammasomes in inflammatory cascades implicated in the pathogenesis of several diseases. Here, we review inflammasome activation, its mechanism of action, and its role in CVD. In particular, we describe the role of inflammasomes in rheumatic heart disease, Kawasaki disease, familial Mediterranean fever, ankylosing spondylitis, and rheumatoid arthritis as exemplars to illustrate pathobiological mechanisms and the potential for targeting inflammasomes for therapeutic benefit. Full article
(This article belongs to the Special Issue New Molecular Mechanisms and Markers in Inflammatory Disorders, 3rd Edition)
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24 pages, 1598 KiB  
Review
Exploring the Role of Gut Microbiota and Probiotics in Acute Pancreatitis: A Comprehensive Review
by Enrico Celestino Nista, Simone Parello, Mattia Brigida, Giulio Amadei, Angela Saviano, Sara Sofia De Lucia, Carmine Petruzziello, Alessio Migneco and Veronica Ojetti
Int. J. Mol. Sci. 2025, 26(7), 3433; https://doi.org/10.3390/ijms26073433 - 6 Apr 2025
Viewed by 715
Abstract
Acute pancreatitis (AP) is a common and potentially severe gastrointestinal condition characterized by acute inflammation of the pancreas. The pathophysiology of AP is multifactorial and intricate, involving a cascade of events that lead to pancreatic injury and systemic inflammation. The progression of AP [...] Read more.
Acute pancreatitis (AP) is a common and potentially severe gastrointestinal condition characterized by acute inflammation of the pancreas. The pathophysiology of AP is multifactorial and intricate, involving a cascade of events that lead to pancreatic injury and systemic inflammation. The progression of AP is influenced by many factors, including genetic predispositions, environmental triggers, and immune dysregulation. Recent studies showed a critical involvement of the gut microbiota in shaping the immune response and modulating inflammatory processes during AP. This review aims to provide a comprehensive overview of the emerging role of gut microbiota and probiotics in AP. We analyzed the implication of gut microbiota in pathogenesis of AP and the modification during an acute attack. The primary goals of microbiome-based therapies, which include probiotics, prebiotics, antibiotics, fecal microbiota transplantation, and enteral nutrition, are to alter the composition of the gut microbial community and the amount of metabolites derived from the microbiota. By resetting the entire flora or supplementing it with certain beneficial organisms and their byproducts, these therapeutic approaches aim to eradicate harmful microorganisms, reducing inflammation and avoiding bacterial translocation and the potential microbiota-based therapeutic target for AP from nutrition to pre- and probiotic supplementation to fecal transplantation. Full article
(This article belongs to the Special Issue New Molecular Mechanisms and Markers in Inflammatory Disorders, 3rd Edition)
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19 pages, 2300 KiB  
Review
TANK-Binding Kinase 1 in the Pathogenesis and Treatment of Inflammation-Related Diseases
by Lu Hui, Xiaolin Chen, Mengke Huang, Yongmei Jiang and Ting Liu
Int. J. Mol. Sci. 2025, 26(5), 1941; https://doi.org/10.3390/ijms26051941 - 24 Feb 2025
Viewed by 647
Abstract
TANK-binding kinase 1 (TBK1) is a key signaling kinase involved in innate immune and inflammatory responses. TBK1 drives immune cells to participate in the inflammatory response by activating the NF-κB and interferon regulatory factor signaling pathways in immune cells, promoting the expression of [...] Read more.
TANK-binding kinase 1 (TBK1) is a key signaling kinase involved in innate immune and inflammatory responses. TBK1 drives immune cells to participate in the inflammatory response by activating the NF-κB and interferon regulatory factor signaling pathways in immune cells, promoting the expression of pro-inflammatory genes, and regulating immune cell function. Thus, it plays a crucial role in initiating a signaling cascade that establishes an inflammatory environment. In inflammation-related diseases, TBK1 acts as a bridge linking inflammation to immunity, metabolism, or tumorigenesis, playing an important role in the pathogenesis of immune-mediated inflammatory diseases, metabolic, inflammatory syndromes, and inflammation-associated cancers by regulating the activation of inflammatory pathways and the production of inflammatory cytokines in cells. In this review, we focused on the mechanisms of TBK1 in immune cells and inflammatory-related diseases, providing new insights for further studies targeting TBK1 as a potential treatment for inflammation-related diseases. Thus, optimizing and investigating highly selective cell-specific TBK1 inhibitors is important for their application in these diseases. Full article
(This article belongs to the Special Issue New Molecular Mechanisms and Markers in Inflammatory Disorders, 3rd Edition)
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