Journal of Inflammation Research
The following Article Collections/ Thematic Series are currently open for submissions:
Genetic and non-genetic inflammation networks in major human diseases
Inflammation is an adaptive response and integral part of animal biology against a myriad of factors including infection, trauma, and disease. Considerable progress has been made in understanding the cellular and molecular events that are involved in the acute inflammatory response to infection and, to a lesser extent, tissue injury and chronic inflammation.
Numerous studies have shown how the clinical manifestation of inflammation can also be pathological and prime the tissue niche for the progression of myriad complex diseases such as cancer, microbial resistance, autoimmune disorders, and gut microbiota dysbiosis.
Interestingly, several genome-wide association studies (GWAS), whole-exome sequencing (WES), and single cell-based technologies have highlighted how rare genetic mutations or variations modulate the susceptibility of an individual to infectious pathogens, such as Mycobacterium tuberculosis (TB), Human Immunodeficiency Virus (HIV), and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), by influencing pathological inflammation at a genetic level.
In addition to the genetic determinants, inflammation can also be triggered by multiple non-genetic factors including the microbiome, toxic compounds, diet, and stress, which affect the epigenome and secretome of the tissue microenvironment.
Altogether, these genetic and non-genetic networks in inflammatory diseases have long been established in several clinical and epidemiological studies. However, we still lack a significant understanding of causal links and strategic explanations for the interaction between genome, epigenome, microbiome, metabolome, and inflammatome. Therefore, we need a cohesive approach focusing on both genetic and non-genetic determinants to curb pathological inflammation.
In this article collection, we welcome the submission of original research articles and reviews related to, but not limited to:
1. The understanding of mechanisms of inflammation and inflammatory responses in a variety of diseases.
2. Molecular and computational methodologies to identify new genetic variants linked to the cause and consequences of inflammatory diseases.
3. Novel molecular approaches to identify targets of translational and pathological inflammation.
The deadline for submitting manuscripts is 15 December 2023.
Please submit your manuscript on our website, quoting the promo code PQCII to indicate that your submission is for consideration in this Article Collection.
Unraveling the Complex Relationship Between Inflammation, Diabetes, and Obesity: A Comprehensive Exploration
Dove Medical Press is pleased to invite you to submit your research to an upcoming Article Collection in the Journal of Inflammation Research on "Unraveling the Complex Relationship Between Inflammation, Diabetes, and Obesity: A Comprehensive Exploration", organized by Guest Advisor Dr. Nasser Rizk (Qatar University, Qatar).
Diabetes and obesity are two of the most prevalent chronic metabolic diseases worldwide, with estimates indicating that more than 420 million individuals worldwide are living with diabetes and over 650 million individuals are obese or overweight. Both conditions have significant impacts on health and quality of life, and they are associated with an increased risk of numerous comorbidities, including cardiovascular disease, stroke, fatty liver, and certain types of cancer. However, despite the significant advances in our understanding of the pathophysiology of these conditions, the precise mechanisms by which they develop and progress remain incompletely understood.
Recent research has highlighted the role of inflammation in the development and progression of both obesity and diabetes. Inflammation is a complex process that involves the activation of various immune cells, cytokines, and other inflammatory mediators in response to tissue damage, infection, or other stimuli. While inflammation is typically a protective response that helps to clear pathogens and promote tissue repair, chronic low-grade inflammation can contribute to metabolic abnormalities, including insulin resistance, impaired glucose metabolism, and dyslipidaemia. Even though there has been a lot of progress achieved in the fields of obesity, diabetes, and inflammation, many concerns about the underlying molecular mechanisms of these chronic illnesses still need to be answered. The recent emergence of immunometabolism as an innovative field in medical studies demonstrates the interconnectedness of various fields and the centrality of immunology in health and disease.
In individuals with obesity, adipose tissue is a significant source of pro-inflammatory cytokines such as tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6). Adipose tissue inflammation is thought to contribute to insulin resistance and the development of type 2 diabetes by impairing insulin signaling and promoting the release of free fatty acids into the circulation. Inflammation has also been implicated in the pathogenesis of type 1 diabetes, with evidence suggesting that inflammatory cells and cytokines contribute to beta-cell destruction and the loss of insulin secretion. While the link between inflammation and metabolic abnormalities is becoming increasingly clear, the precise mechanisms involved in this relationship are still not fully understood. Moreover, understanding the process by which inflammation is reduced is just as crucial for predicting the course of a disease as learning how it is initially triggered. However, recent research has shed light on some potential mechanisms, including the activation of the nuclear factor kappa B (NF-κB) pathway, the induction of endoplasmic reticulum (ER) stress, and the modulation of gut microbiota. Furthermore, several studies have demonstrated the potential of anti-inflammatory agents, such as non-steroidal anti-inflammatory drugs (NSAIDs), to improve metabolic outcomes in individuals with diabetes and obesity.
Potential subtopics related to recurrent miscarriage include (but are not limited to):
• The role of adipose tissue inflammation in the development of obesity and diabetes
• The link between inflammation [local and systemic] and insulin resistance
• The impact of inflammation on beta-cell function and insulin secretion
• The potential of anti-inflammatory agents as therapeutic interventions for diabetes and obesity
• The relationship between inflammation, gut microbiota, and metabolic health
• The role of exercise and dietary interventions in reducing inflammation and improving metabolic outcomes in individuals with diabetes and obesity.
Overall, inflammation is a crucial player in the pathogenesis of diabetes and obesity, and a better understanding of the mechanisms involved could potentially lead to the development of novel therapeutic interventions. This Article Collection aims to explore the role of inflammation in the pathogenesis of diabetes and obesity, with a focus on the latest research findings and potential therapeutic interventions. We invite original research articles, reviews, and perspectives that explore this complex relationship, and we hope that this Article Collection will contribute to the ongoing efforts to improve the prevention and treatment of these prevalent chronic diseases.
Please submit your manuscript on our website, quoting the promo code OBCZU to indicate that your submission is for consideration in this Article Collection.
Takayasu Arteritis: Insights Into Pathogenesis, Disease Assessment, Treatment, and Outcomes
Dove Medical Press is pleased to invite you to submit your research to an upcoming Article Collection on "Takayasu Arteritis: Insights Into Pathogenesis, Disease Assessment, Treatment, and Outcomes", in the Journal of Inflammation Research.
Takayasu arteritis (TAK) is a rare large vessel vasculitis (LVV). Although more common in Asia, TAK is diagnosed worldwide. The pathology of TAK is a granulomatous inflammation of the aorta and its major branches. Limited studies available from mostly Europe and North America have revealed an increased mortality risk with TAK relative to the general population.
Much remains to be understood about TAK. The assessment of disease activity is challenging. In many instances, TAK sets in insidiously. Patients with TAK might simply be diagnosed incidentally upon the detection of asymmetry of pulses or blood pressure. On the other hand, it can also present with prominent constitutional symptoms without pulse loss at the onset or can present with severe ischemic manifestations such as stroke, myocardial infarction, or vision loss. While the pathology is an inflammatory vasculitis, in many instances, traditional inflammatory markers such as C-reactive protein (CRP) are not elevated. In such instances, 18-F fluorodeoxyglucose PET can identify active TAK even in the absence of CRP elevation. Of late, novel PET ligands such as SST2R and FAPI have been explored as denoting macrophage infiltration or fibroblast activation in the arterial wall.
The treatment of TAK is also challenging. Despite the key pathology of vessel wall inflammation, no immunosuppressive agent has been identified to be effective in a clinical trial of TAK. There is a need to explore newer therapies or therapeutic strategies in TAK, which could include the exploration of adjunctive therapies that affect arterial wall fibrosis (which is a prominent histopathological feature of TAK) in addition to the targeting of inflammation.
This Article Collection invites original and review articles of translational relevance in TAK, including those related to novel blood and imaging biomarkers of disease activity and arterial wall damage, novel therapeutic strategies, and biomarkers of long-term outcomes in TAK.
All manuscripts submitted to this Article Collection will undergo a full peer-review; the Guest Advisor will not be handling the manuscripts. Please review the journal’s aims and scope and author submission instructions prior to submitting a manuscript.
Please submit your manuscript on our website, quoting the promo code AHYGD to indicate that your submission is for consideration in this Article Collection. Promo codes are used to identify articles that belong to a specific Collection, so it is important to use the correct code.
The deadline for submitting a manuscript is 15 May 2024. If you have questions, please contact Krista Thom at [email protected].
Prof. Durga Prasanna Misra, Associate Professor, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, India
Call For Papers
To see where the Journal of Inflammation Research is indexed online view the Journal Metrics.
What is the advantage to you of publishing in the Journal of Inflammation Research?
- It is an open access journal which means that your paper is available to anyone in the world to download for free directly from the Dove website.
- Although the Journal of Inflammation Research receives a lot of papers, unlike many traditional journals, your paper will not be rejected due to lack of space. We are an electronic journal and there are no limits on the number or size of the papers we can publish.
- The time from submission to a decision being made on a paper can, in many journals, take some months and this is very frustrating for authors. The Journal of Inflammation Research has a quicker turnaround time than this. Generally peer review is complete within 3-4 weeks and the editor’s decision within 2-14 days of this. It is therefore very rare to have to wait more than 6 weeks for first editorial decision.
- Many authors have found that our peer reviewer’s comments substantially add to their final papers.
To recover our editorial and production costs and continue to provide our content at no cost to readers we charge authors or their institution an article publishing charge.
The Journal of Inflammation Research is indexed on PubMed Central (title abbreviation: J Inflamm Res). All published papers in this journal are submitted to PubMed for indexing straight away.
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Professor Ning Quan
Journal of Inflammation Research
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