Oxidative Medicine and Cellular Longevity

Crosstalk Between the Inflammatory Immune Response and Oxidative Stress in Tumor Microenvironment


Publishing date
01 May 2023
Status
Closed
Submission deadline
23 Dec 2022

Lead Editor

1Zhejiang University School of Medicine, Hangzhou, China

2Naval Medical Center Portsmouth, Portsmouth, USA

3Fudan University, Shangha, Shanghai, China

4Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, China

5Zhejiang University, Hangzhou, China

This issue is now closed for submissions.

Crosstalk Between the Inflammatory Immune Response and Oxidative Stress in Tumor Microenvironment

This issue is now closed for submissions.

Description

Cancer represents the leading cause of death in countries around the world and a significant barrier to increasing life expectancy. The inflammatory immune response is a hallmark of cancer. Immuno-inflammatory responses have a great impact on cancer development in various ways, including affecting cell proliferation, modulating the tumor microenvironment (TME), and secreting pro- or antitumor cytokines. Drugs that boost host immunity are a hot spot in the fight against cancer, while anti-inflammatories have also been suggested as a way to prevent cancer over the past few decades. These conflicting effects have momentous implications for potential antitumor strategies aimed at modulating the level of inflammatory immune responses. Oxidative stress is a physiological process formed by the accumulation of free radicals derived from the changing environment such as mitochondria dysfunction and inflammation. Reactive oxygen species (ROS) are essential free radicals that can exacerbate oxidative stress and aggravate tissue dysfunction. At equilibrium, a dynamic balance exists between the generation and scavenging of ROS in vivo.

However, the excess production of ROS has an effect on cells, leading to protein misfolding, chromosome instability, and among others. Oxidative stress and the corresponding oxidative damage are key players in cancer formation and progression. Both extrinsic and intrinsic ROS can lead to increased cellular oxidative stress. Excessive amounts of ROS lead to damage and modification of cellular macromolecules, most importantly the mutation of genomic DNA, triggering the initiation of cancers. In addition, oxidative stress also regulates gene expression of downstream pathways such as DNA repair, anti-oxidation, and cell proliferation. However, at high levels, ROS may hinder tumorigenesis, which is attributed to the induction of cell death and severe cellular damage. Therefore, cancer cells, especially in the early stages of tumorigenesis, need to confront high levels of ROS. These contradictory findings make the role of ROS a mystery. In addition, few biomarkers have been used to better understand how oxidative stress is implicated in cancer pathophysiology to date. Interestingly, oxidative stress, inflammation immune response, and tumor progression are intricately intertwined and mutually reinforcing. Chronic oxidative stress can elicit irritation and lead to a chronic inflammatory state, which in turn may boost tumor development. Meanwhile, the inflammatory reaction also produces abundant substances in surrounding tissues that directly or indirectly induce oxidative stress, ultimately leading to tumor formation. The suppression of host antitumor immunity exhibits a critical role in tumor progression, while oxidative stress or chronic inflammatory reaction is known to restrain the cell-mediated immune system. It is also evident that the active tumor itself and many components of the TME cause various inflammatory mediators and ROS, contributing to an environment of chronic oxidative stress. Numerous studies have demonstrated the importance of tumor and TME-induced oxidative stress in suppressing immune responses.

This Special Issue aims to promote research related to the interplay process of inflammatory immune response and oxidative stress in tumorigenesis and progression, uncovering the underlying molecular mechanisms and promising therapeutic targets for cancer. We welcome both original research and review articles.

Potential topics include but are not limited to the following:

  • The relationship between oxidative stress and tumor formation and development.
  • The role inflammatory immune response plays in tumor formation and development.
  • The crosstalk between the inflammatory immune response and oxidative stress in cancer pathophysiology, including the transformation of a normal cell to a tumor cell, tumor cell survival, proliferation, chemoresistance, radioresistance, invasion, and angiogenesis.
  • Emerging targets or intervention options for cancer therapy by modulating oxidative stress or inflammatory immune response.
  • Biomarkers regarding oxidative stress and/or inflammatory immune response for cancer diagnosis, treatment, and prognosis
Oxidative Medicine and Cellular Longevity
 Journal metrics
See full report
Acceptance rate8%
Submission to final decision133 days
Acceptance to publication34 days
CiteScore10.100
Journal Citation Indicator-
Impact Factor-
 Submit Evaluate your manuscript with the free Manuscript Language Checker

We have begun to integrate the 200+ Hindawi journals into Wiley’s journal portfolio. You can find out more about how this benefits our journal communities on our FAQ.