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Oxidative Stress and Inflammation in Diabetic Complications
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Oxidative Stress and Inflammation in Diabetic Complications

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: closed (30 August 2023) | Viewed by 4694

Special Issue Editors

Dr. Tiziana Genovese

E-Mail Website
Guest Editor
Department of Chemical, Biological, Pharmaceutical and Environmental Science, University of Messina, 98122 Messina, Italy
Interests: antioxidant; anti-inflammatory
Special Issues, Collections and Topics in MDPI journals
Dr. Roberta Fusco

E-Mail Website
Guest Editor
Department of Chemical, Biological, Pharmaceutical and Environmental Science, University of Messina, 98122 Messina, Italy
Interests: biochemistry; molecular mechanism; oxidative stress; endometriosis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Increased prevalence of insulin resistance, a prediabetic condition, and type 2 diabetes is a major health concern all over the world. As per WHO estimates, it is expected that by 2030, the number of patients with diabetes will be more than double. Progressive deterioration in metabolic control with existing therapeutic modalities necessitates better understanding and newer therapeutic interventions for the effective management of diabetes.

Oxidative stress and inflammation affect a multitude of cellular responses in various organ systems, and progression of insulin-resistance is known to be associated with chronic systemic inflammation and increased oxidative stress. The positive feedback cycle involving chronic systemic inflammation, oxidative stress, and progression of insulin resistance contributes to several diabetes-associated complications, including cardiovascular diseases, nephropathy, neuropathy, retinopathy, urological diseases, and cancer.

This Special Issue on “Oxidative Stress and Inflammation in Diabetic Complications” aims to stimulate comprehensive research in this field. We will accept articles on the pathophysiology of diabetes, molecular basis, imaging, and strategies including pharmacological and non-pharmacological approaches.

Dr. Tiziana Genovese
Dr. Roberta Fusco
Guest Editors

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 submissions that pass pre-check are 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

  • insulin resistance
  • oxidative stress
  • inflammation
  • diabetic complications
  • diabetes

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Published Papers (2 papers)

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Research

12 pages, 951 KiB  
Article
Associations between Inflammation, Hemoglobin Levels, and Coronary Artery Disease in Non-Albuminuric Subjects with and without Type 2 Diabetes Mellitus
by Javier Donate-Correa, Ernesto Martín-Núñez, Carmen Mora-Fernández, Ainhoa González-Luis, Alberto Martín-Olivera and Juan F. Navarro-González
Int. J. Mol. Sci. 2023, 24(18), 14131; https://doi.org/10.3390/ijms241814131 - 15 Sep 2023
Cited by 1 | Viewed by 2169
Abstract
In this cross-sectional study, we evaluated the associations of inflammation and hemoglobin with coronary artery disease (CAD) in subjects with type 2 diabetes mellitus (T2DM) and preserved kidney function. We recruited 638 participants—254 with T2DM—subjected to coronary angiography with no known cardiovascular disease, [...] Read more.
In this cross-sectional study, we evaluated the associations of inflammation and hemoglobin with coronary artery disease (CAD) in subjects with type 2 diabetes mellitus (T2DM) and preserved kidney function. We recruited 638 participants—254 with T2DM—subjected to coronary angiography with no known cardiovascular disease, normal glomerular filtration rates, and without albuminuria. The hemoglobin and serum levels of inflammatory markers, including high-sensitivity C-reactive protein (hs-CRP), were measured. Multivariable analyses showed that inflammatory markers were not related to the severity of the stenosis in the group of subjects with diabetes. Conversely, inflammatory cytokines and albuminuria were directly related to the percentage of stenosis in subjects without T2DM (R2 = 0.038, p < 0.001). Patients with diabetes presented lower hemoglobin levels, particularly in those who also had significant CAD (14.4 [13.6–15.1] vs. 13.6 [12.2–14.8] g/dL, p = 0.03). Similarly, hemoglobin levels and albuminuria were inversely related to the severity of stenosis exclusively in subjects with diabetes, even after adjusting for multiple confounding factors (R2 = 0.081, p < 0.001). We conclude that reductions in hemoglobin levels in subjects with T2DM and normoalbuminuria may constitute a more relevant risk factor for CAD than inflammation. Full article
(This article belongs to the Special Issue Oxidative Stress and Inflammation in Diabetic Complications)
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20 pages, 3394 KiB  
Article
Paracrine Signals in Calcified Conditioned Media Elicited Differential Responses in Primary Aortic Vascular Smooth Muscle Cells and in Adventitial Fibroblasts
by Amber M. Kennon and James A. Stewart, Jr.
Int. J. Mol. Sci. 2023, 24(4), 3599; https://doi.org/10.3390/ijms24043599 - 10 Feb 2023
Viewed by 1764
Abstract
Our goal was to determine if paracrine signals from different aortic layers can impact other cell types in the diabetic microenvironment, specifically medial vascular smooth muscle cells (VSMCs) and adventitial fibroblasts (AFBs). The diabetic hyperglycemic aorta undergoes mineral dysregulation, causing cells to be [...] Read more.
Our goal was to determine if paracrine signals from different aortic layers can impact other cell types in the diabetic microenvironment, specifically medial vascular smooth muscle cells (VSMCs) and adventitial fibroblasts (AFBs). The diabetic hyperglycemic aorta undergoes mineral dysregulation, causing cells to be more responsive to chemical messengers eliciting vascular calcification. Advanced glycation end-products (AGEs)/AGE receptors (RAGEs) signaling has been implicated in diabetes-mediated vascular calcification. To elucidate responses shared between cell types, pre-conditioned calcified media from diabetic and non-diabetic VSMCs and AFBs were collected to treat cultured murine diabetic, non-diabetic, diabetic RAGE knockout (RKO), and non-diabetic RKO VSMCs and AFBs. Calcium assays, western blots, and semi-quantitative cytokine/chemokine profile kits were used to determine signaling responses. VSMCs responded to non-diabetic more than diabetic AFB calcified pre-conditioned media. AFB calcification was not significantly altered when VSMC pre-conditioned media was used. No significant changes in VSMCs signaling markers due to treatments were reported; however, genotypic differences existed. Losses in AFB α-smooth muscle actin were observed with diabetic pre-conditioned VSMC media treatment. Superoxide dismutase-2 (SOD-2) increased with non-diabetic calcified + AGE pre-conditioned VSMC media, while same treatment decreased diabetic AFBs levels. Overall, non-diabetic and diabetic pre-conditioned media elicited different responses from VSMCs and AFBs. Full article
(This article belongs to the Special Issue Oxidative Stress and Inflammation in Diabetic Complications)
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