Guest Editor(s)
Assist. Prof. Divya Gopinath
Email: drdivyakmenon@gmail.com
Affiliation: 1. ollege of Dentistry, Ajman University, Ajman, United Arab Emirates
2. Centre of Medical and Bio-Allied Health Sciences Research, Ajman University, Ajman, United Arab Emirates
Homepage:
Research Interests: oral and maxillofacial pathology, oral medicine, histopathology, oral diseases, oral pathology, oral biology, molecular virology, virology, molecular cell biology, evidence based medicine
Dr. Qi Wang
Email: drwang71111@sjtu.edu.cn
Affiliation: Department of Oncology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China
Homepage:
Research Interests: tumor microenvironment, multi-omics, metabolic heterogeneity, cytokine
Dr. Hengrui Liu
Email: hl546@cam.ac.uk
Affiliation: Early Cancer Institute, Department of Oncology, University of Cambridge, Cambridge, United Kingdom
Homepage:
Research Interests: cancer biology, precision medicine, biochemistry, genomics
Assoc. Prof. Zhirui Zeng
Email: zengzhirui@gmc.edu.cn
Affiliation: College of Basic Medicine, Guizhou Medical University, Guiyang, China
Homepage:
Research Interests: bioinformatics, biomarker discovery, digestive system tumors, molecular mechanisms, small molecule inhibitors, target site design, pharmacological effects
Summary
Inflammation is a core defense response of the body to infection, injury, or stress. However, uncontrolled chronic inflammation is closely associated with the development and progression of tumors, autoimmune diseases, metabolic syndrome, and neurodegenerative disorders. Among the numerous regulatory factors within the inflammatory network, cytokines act as signaling hubs. Through complex synergistic, antagonistic, or cascade-amplifying effects, they precisely regulate the recruitment, activation, and resolution of immune cells. Nevertheless, a purely pro-inflammatory or anti-inflammatory perspective can no longer adequately explain the dynamically evolving inflammatory phenotypes observed during disease progression. In recent years, accumulating evidence has shown that cytokines do not function in isolation but instead form a highly intertwined interaction network. Crosstalk in signaling pathways frequently occurs among different cytokine families, and even the same cytokine can exhibit entirely opposite functions depending on the microenvironment. Imbalances in these interactions often serve as the critical turning point where acute inflammation transitions into chronic pathological states.
This special issue aims to gather the latest research findings on how cytokine interactions shape inflammation-related aspects of diseases, with a focus on the following directions:
(1) the dynamic reorganization principles of cytokine networks under physiological or pathological conditions;
(2) key node cytokines and their upstream and downstream regulatory mechanisms;
(3) intervention strategies based on cytokine interaction networks. We encourage the use of multi-omics, single-cell analysis, in vivo animal models, and clinical sample validation as multi-level research approaches, in order to re-understand the central role of inflammation in disease pathogenesis from the higher dimension of "interaction networks."
Keywords
inflammation, cytokine, cancer, metabolic syndrome, immune