Journal of Immunology Research

Cell Death Signaling and Mechanisms of Systemic Inflammation


Publishing date
01 Dec 2021
Status
Published
Submission deadline
23 Jul 2021

Lead Editor

1Nanchang University, Nanchang, China

2Indiana University School of Medicine, Indianapolis, USA

3Peking Union Medical College, Beijing, China


Cell Death Signaling and Mechanisms of Systemic Inflammation

Description

Systemic inflammation is defined as a multi-syndrome pathological process and is characterized by the increase of total inflammatory reactivity. Systemic inflammation is attributed to both infectious and non-infectious causes and is classically associated with acute and chronic diseases. Moreover, it is associated with a far higher risk of adverse outcomes and potentially with long-term multi-organ damage, including the lungs, liver, and kidneys.

Various types of cells are involved in the pathology of systemic inflammation-induced injury. The accumulation of pro-inflammatory cytokines causes damage to parenchymal cells and immune cells via different forms of cell death, including apoptosis, pyroptosis, and necrosis. In particular, pyroptosis has been defined as a specific programmed cell death characterized by the release of inflammatory cytokines. Appropriate pyroptosis can minimize tissue damage, but severe pyroptosis can aggravate secondary injury of the tissue. However, the mechanisms underlying multicellular and tissue damage from systemic inflammation remain largely unknown, and no drug therapies have yet shown clear benefit in patients with severe sepsis and multiple organ failure/multiple organ dysfunction syndrome.

The aim of this Special Issue is to encourage submissions, including original research, clinical studies, and review articles, that contribute innovative knowledge to further our understanding of the signaling and mechanisms of systemic inflammation-induced cell, tissue, and organ injury in multiple diseases.

Potential topics include but are not limited to the following:

  • Animal, cellular, and molecular models of systemic inflammation-induced multiple organ failure/multiple organ dysfunction syndrome
  • Inflammatory mediator-induced cell death in sepsis, trauma, pancreatitis, mesenteric infarction, and chemical-induced acute lung/kidney/liver injury and multiple organ failure
  • Inflammatory mediator-induced cell death in the context of chronic inflammation-induced organ injury, including atherosclerosis, rheumatoid arthritis, and chronic liver disease
  • Discovery of novel biomarkers and mechanisms in animal models or patients with acute/chronic inflammation-induced injury
  • Identification and pharmacological studies of bioactive molecules that target systemic inflammation induced-damage
  • Signaling and mechanisms of inflammation and tissue damage caused by dysbacteriosis
  • Treatment of dysbacteriosis-induced tissue damage using probiotics and prebiotics via monitoring bacterial changes using metagenomics, metabolomics, and transcriptomics
  • Exogenous or endogenous inflammatory mediator-induced vascular endothelial activation and dysfunction in organ injury
  • Compounds that act on endothelial activation and dysfunction to alleviate systemic inflammation and organ injury
  • Apoptosis, pyroptosis, and necrosis signaling in parenchymal cells induced by systemic inflammation
  • Signaling and mechanisms of apoptosis, pyroptosis, and necrosis in macrophages, neutrophils. and other immune cells
  • Inhibition of systemic inflammation-induced cell apoptosis, pyroptosis, and necrosis by novel small molecular compounds
Journal of Immunology Research
 Journal metrics
See full report
Acceptance rate11%
Submission to final decision121 days
Acceptance to publication27 days
CiteScore6.000
Journal Citation Indicator0.560
Impact Factor4.1
 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.