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Biology
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Pathophysiology of Chronic Inflammatory Diseases
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Pathophysiology of Chronic Inflammatory Diseases

A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Physiology".

Deadline for manuscript submissions: 1 December 2025 | Viewed by 813

Special Issue Editor

Dr. Vincent Yuan

E-Mail Website
Guest Editor
Department of Otolaryngology, University of Pittsburgh Medical Center, 600 Grant St, Pittsburgh, PA 15219, USA
Interests: chronic inflammatory diseases; immune-mediated hearing disorders; macrophage and T cell biology; inflammasome activation; biomarkers; therapeutic targets
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Chronic inflammatory diseases represent a significant global health challenge, affecting millions worldwide. These conditions, including autoimmune disorders, metabolic syndromes, and persistent infections, are characterized by sustained inflammation leading to tissue damage and organ dysfunction. Despite advances in understanding their mechanisms, the complexity of these diseases calls for further investigation to uncover new therapeutic avenues.

This Special Issue aims to explore the molecular, cellular, and systemic processes underlying chronic inflammation, offering insights into pathogenesis, diagnosis, and treatment strategies. We invite contributions addressing key areas such as immune cell dysregulation, cytokine signaling, and inflammasome activation, as well as the role of genetic, epigenetic, and environmental factors. Research on metabolic disturbances, oxidative stress, and their links to chronic inflammation is particularly welcome.

In this Special Issue, original research articles and reviews are encouraged. Topics may include (but are not limited to):

  • Mechanisms of immune cell activation and dysregulation;
  • Genetic and epigenetic factors in chronic inflammation;
  • Biomarkers for diagnosis and disease monitoring.

We look forward to your valuable contributions.

Dr. Vincent Yuan
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biology is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • chronic inflammation
  • autoimmune diseases
  • cytokines
  • inflammasome
  • metabolic dysfunction
  • oxidative stress
  • biomarkers
  • epigenetics
  • personalized medicine
  • therapeutic targets

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Published Papers (2 papers)

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Research

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15 pages, 1133 KiB  
Communication
Anti-Inflammatory Mechanism Prediction of Sinomenine Based on Network Pharmacology and Its Biological Activity Verification
by Da Song, Afsar Khan, Ming-Hong Dong, Chuan-Wen Lei, Ting-Ting Feng, Ying Zhou and Xin Wei
Biology 2025, 14(5), 543; https://doi.org/10.3390/biology14050543 (registering DOI) - 13 May 2025
Abstract
Mechanism analyses of traditional Chinese medicine (TCM) components have always been a challenge in pharmaceutical research. As for the well-known medicinal isoquinoline from the plant Sinomenium acutum, the possible mechanism of the compound sinomenine for targeting anti-inflammatory activities is rarely involved and [...] Read more.
Mechanism analyses of traditional Chinese medicine (TCM) components have always been a challenge in pharmaceutical research. As for the well-known medicinal isoquinoline from the plant Sinomenium acutum, the possible mechanism of the compound sinomenine for targeting anti-inflammatory activities is rarely involved and is still unclear. In this article, a network pharmacological strategy collected the common targets between major inflammation models and the compound sinomenine. The results suggested that JAK2, MMP9, PTGS2, JAK1, MPO, and JAK3 are the key targets between sinomenine and the main inflammatory indications. Then, bioactivity validation was used to further clarify the possible anti-inflammatory activity of sinomenine by ELISA analysis. At the tested concentration on LPS-induced RAW 264.7 cells, sinomenine significantly inhibited the expression of inflammatory factors NO, TNF-a, and IL-6, some of which were equivalent to the positive drug dexamethasone. Meanwhile, RT-qPCR experiments found that sinomenine clearly affected the expression of JAK/STAT pathway factors, including JAK1, STAT3, PTGS2, and IL-6. Molecular docking was further used to speculate on the binding mechanism of the compound sinomenine with key proteins in the JAK/STAT pathway. This study integrated network pharmacology, in vitro activity assessment, mechanism validation, and molecular docking to identify the key targets and potential pathway for sinomenine in anti-inflammatory treatment. Full article
(This article belongs to the Special Issue Pathophysiology of Chronic Inflammatory Diseases)
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Review

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29 pages, 3987 KiB  
Review
Tryptophan-2,3-Dioxygenase as a Therapeutic Target in Digestive System Diseases
by Zhengsen Wang, Xianxian Xie, Yu Xue and Yixuan Chen
Biology 2025, 14(3), 295; https://doi.org/10.3390/biology14030295 - 15 Mar 2025
Viewed by 654
Abstract
Tryptophan (Trp) is an essential amino acid that must be acquired exclusively through dietary intake. The metabolism of tryptophan plays a critical role in maintaining immune homeostasis and tolerance, as well as in preventing excessive inflammatory responses. Tryptophan-2,3-dioxygenase (TDO2) is a tetrameric heme [...] Read more.
Tryptophan (Trp) is an essential amino acid that must be acquired exclusively through dietary intake. The metabolism of tryptophan plays a critical role in maintaining immune homeostasis and tolerance, as well as in preventing excessive inflammatory responses. Tryptophan-2,3-dioxygenase (TDO2) is a tetrameric heme protein and serves as one of the pivotal rate-limiting enzymes in the first step of tryptophan metabolism. Dysregulation of TDO2 expression has been observed in various digestive system diseases, encompassing those related to the oral cavity, esophagus, liver, stomach, pancreas, and colon and rectum. Digestive system diseases are the most common clinical diseases, with complex clinical manifestations and interrelated symptoms, and have become a research hotspot in the field of medicine. Studies have demonstrated that aberrant TDO2 expression is closely associated with various clinical manifestations and disease outcomes in patients with digestive system disorders. Consequently, TDO2 has garnered increasing recognition as a promising therapeutic target for digestive system diseases in recent years, attracting growing attention. This article provides a brief overview of the role of TDO2 in the tryptophan pathway, emphasizing its significant involvement in diseases of the digestive system. Strategies targeting TDO2 through specific inhibitors suggest considerable promise in enhancing therapeutic outcomes for digestive diseases. Thus, this review concludes by discussing recent advancements in the development of TDO2 inhibitors. We believe that targeted inhibition of TDO2 combined with immunotherapy, the screening of a large number of natural products, and the assistance of artificial intelligence in drug design will be important directions for developing more effective TDO2 inhibitors and improving treatment outcomes in the future. Full article
(This article belongs to the Special Issue Pathophysiology of Chronic Inflammatory Diseases)
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