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Special Issue "TNF and ROS Crosstalk in Inflammation"

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

Deadline for manuscript submissions: 30 April 2021.

Special Issue Editor

Special Issue Information

Tumor necrosis factor-α (TNF-α) is a representative pro-inflammatory cytokine that contributes to host defense by inducing a wide variety of cellular responses, including cell growth, differentiation, inflammatory responses, and cell death. TNF-α also promotes production of reactive oxygen species (ROS) as second messengers to stimulate ROS-responsive signaling pathways. Conversely, previous studies demonstrated that signalling mechanisms activated by ROS upregulates the expression of TNF-α. Accumulating evidence indicates the involvement of intricate crosstalk between TNF-α and ROS in the pathological process of inflammatory diseases and cancer. Therefore, uncovering the molecular mechanisms of the crosstalk between TNF-α and ROS would lead to a better understanding of the pathogenetic mechanisms of TNF-α- and ROS-related diseases, which may be one of the strategies to overcome these diseases. In this Special Issue, studies of novel signalling mechanisms and pathological process mediated by TNF-α and ROS are welcome.

Dr. Takuya Noguchi
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.

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Published Papers (1 paper)

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Research

Open AccessArticle
Intestinal SIRT1 Deficiency-Related Intestinal Inflammation and Dysbiosis Aggravate TNFα-Mediated Renal Dysfunction in Cirrhotic Ascitic Mice
Int. J. Mol. Sci. 2021, 22(3), 1233; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22031233 - 27 Jan 2021
Viewed by 385
Abstract
In advanced cirrhosis, the TNFα-mediated intestinal inflammation and bacteria dysbiosis are involved in the development of inflammation and vasoconstriction-related renal dysfunction. In colitis and acute kidney injury models, activation of SIRT1 attenuates the TNFα-mediated intestinal and renal abnormalities. This study explores the impacts [...] Read more.
In advanced cirrhosis, the TNFα-mediated intestinal inflammation and bacteria dysbiosis are involved in the development of inflammation and vasoconstriction-related renal dysfunction. In colitis and acute kidney injury models, activation of SIRT1 attenuates the TNFα-mediated intestinal and renal abnormalities. This study explores the impacts of intestinal SIRT1 deficiency and TNFα-mediated intestinal abnormalities on the development of cirrhosis-related renal dysfunction. Systemic and renal hemodynamics, intestinal dysbiosis [cirrhosis dysbiosis ratio (CDR) as marker of dysbiosis], and direct renal vasoconstrictive response (renal vascular resistance (RVR) and glomerular filtration rate (GFR)) to cumulative doses of TNFα were measured in bile duct ligated (BDL)-cirrhotic ascitic mice. In SIRT1IEC-KO-BDL-ascitic mice, the worsening of intestinal dysbiosis exacerbates intestinal inflammation/barrier dysfunction, the upregulation of the expressions of intestinal/renal TNFα-related pathogenic signals, higher TNFα-induced increase in RVR, and decrease in GFR in perfused kidney. In intestinal SIRT1 knockout groups, the positive correlations were identified between intestinal SIRT1 activity and CDR. Particularly, the negative correlations were identified between CDR and RVR, with the positive correlation between CDR and GFR. In mice with advanced cirrhosis, the expression of intestinal SIRT1 is involved in the linkage between intestinal dysbiosis and vasoconstriction/hypoperfusion-related renal dysfunction through the crosstalk between intestinal/renal TNFα-related pathogenic inflammatory signals. Full article
(This article belongs to the Special Issue TNF and ROS Crosstalk in Inflammation)
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