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Special Issue "Molecular Mechanisms of Major Inflammatory Occupational Diseases"

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Immunology".

Deadline for manuscript submissions: 30 March 2022.

Special Issue Editor

Prof. Dr. Shanbeh Zienolddiny
E-Mail Website
Guest Editor
National Institute of Occupational Health, Oslo, Norway
Interests: occupational health; inflammation; molecular genetics; carcinogenesis

Special Issue Information

Dear Colleagues,

Occupational exposure to chemicals and biological agents is common in many work places. Depending on the type of chemical or biological agent, they may lead to adverse health effects in the workers who are handling these agents through the manufacturing, processing, use, or waste handling. Health effects may vary and could include cardiovascular, pulmonary (i.e., COPD, fibrosis, etc.), neurodegenerative diseases, and cancer. However, molecular and cellular mechanisms are unknown but inflammation is a putative common mechanism that operates in these diseases. Knowing mechanisms of disease will help in identification of molecular markers that could be used for prevention and in particular for design of personalized prevention strategies. Molecular and cellular markers of disease are of utmost importance for personalized prevention as these markers are important for personalized diagnostic and treatment strategies. In this Special Issue, the focus will be on the cellular and molecular markers that drive acute inflammation to become chronic inflammtion and so leading to development of inflammatory occupational diseases.

Prof. Dr. Shanbeh Zienolddiny
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 papers will be 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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • occupational health
  • inflammation
  • CVD
  • COPD
  • fibrosis

Published Papers (1 paper)

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Research

Article
Glycolytic Reprogramming in Silica-Induced Lung Macrophages and Silicosis Reversed by Ac-SDKP Treatment
Int. J. Mol. Sci. 2021, 22(18), 10063; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms221810063 - 17 Sep 2021
Viewed by 579
Abstract
Glycolytic reprogramming is an important metabolic feature in the development of pulmonary fibrosis. However, the specific mechanism of glycolysis in silicosis is still not clear. In this study, silicotic models and silica-induced macrophage were used to elucidate the mechanism of glycolysis induced by [...] Read more.
Glycolytic reprogramming is an important metabolic feature in the development of pulmonary fibrosis. However, the specific mechanism of glycolysis in silicosis is still not clear. In this study, silicotic models and silica-induced macrophage were used to elucidate the mechanism of glycolysis induced by silica. Expression levels of the key enzymes in glycolysis and macrophage activation indicators were analyzed by Western blot, qRT-PCR, IHC, and IF analyses, and by using a lactate assay kit. We found that silica promotes the expression of the key glycolysis enzymes HK2, PKM2, LDHA, and macrophage activation factors iNOS, TNF-α, Arg-1, IL-10, and MCP1 in silicotic rats and silica-induced NR8383 macrophages. The enhancement of glycolysis and macrophage activation induced by silica was reduced by Ac-SDKP or siRNA-Ldha treatment. This study suggests that Ac-SDKP treatment can inhibit glycolytic reprogramming in silica-induced lung macrophages and silicosis. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Major Inflammatory Occupational Diseases)
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