Special Issue "Antioxidants and Their Role in the Prevention and Treatment of Chronic Kidney Disease"

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: 31 May 2021.

Special Issue Editors

Dr. Natalia Di Pietro
E-Mail Website
Guest Editor
Department of Medical, Oral and Biotechnological Sciences, University of Chieti-Pescara, Chieti, Italy
Interests: stem cells; biomedical engineering; molecules; extracellular matrix; tissue regeneration; biomaterials
Special Issues and Collections in MDPI journals
Prof. Mario Bonomini
E-Mail Website
Co-Guest Editor
Department of Medicine and Aging, University “G. d’Annunzio” of Chieti-Pescara, Nephrology Unit, SS. Annunziata Hospital, Chieti, Italy
Interests: chronic kidney disease; dialysis; proteomics; red blood cells; end-stage renal disease; uremic toxins; selenium; nutritional molecules
Special Issues and Collections in MDPI journals

Special Issue Information

Dear Colleagues,

You are cordially invited to submit original research articles and reviews for a new Special Issue entitled "Antioxidants and their Role in the Prevention and Treatment of Chronic Kidney Disease."

Oxidative imbalance is widely recognized as a key component of the pathogenesis of chronic kidney disease (CKD). Indeed, it is recognized as a potential cause and consequence of reduced kidney function. Although increased oxidative stress (OS) is unlikely to be the main event of CKD, it is known as a non-traditional risk factor which, along with other modifiable risk factors (such as drug toxicity, urinary tract infections, autoimmune diseases, hyperuricemia, hypertension, dyslipidemia, diabetes, obesity, and inflammation), contributes to the progression of kidney damage.

For these reasons, trying to counteract the increase in reactive oxygen (ROS) and nitrogen (RNS) species using specific antioxidants represents a contemporary challenge.

In this regard, several recent in vitro (cells), ex vivo (tissues and specimens), in vivo (animals) and clinical studies have shown that the use of dietary antioxidants (the Mediterranean diet, polyphenols, curcumin, sulforaphane, quercetin, probiotics, etc.), antioxidant supplements (vitamins C, E, N-acetylcisteine, L-arginine, etc.) or their combination has potential protective effects for CKD and its main complications such as hypertension, atherosclerosis, inflammation, and anemia.

This Special Issue aims to provide a forum collection of the latest in vitro, in vivo, and clinical studies on antioxidants and their biological activities, with a view to a possible therapeutic application for CKD and its complications. Furthermore, as biomarkers of oxidative stress are critical for the development of novel treatments for CKD, studies on the discovery of novel oxidative stress biomarkers and other innovative biomarkers are also welcome.

Dr. Natalia Di Pietro
Prof. Mario Bonomini
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. Antioxidants is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2000 CHF (Swiss Francs). 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

  • Antioxidants
  • Dietary antioxidants
  • Mediterranean diet
  • Chronic kidney disease
  • Dialysis
  • Diabetic kidney disease
  • Cardiovascular diseases
  • Hypertension
  • Inflammation
  • Oxidative stress
  • Biomarkers.

Published Papers (2 papers)

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Research

Open AccessArticle
The Role of Oxidative Stress Markers in Predicting Acute Thrombotic Occlusion of Haemodialysis Vascular Access and Progressive Stenotic Dysfunction Demanding Angioplasty
Antioxidants 2021, 10(4), 569; https://doi.org/10.3390/antiox10040569 - 08 Apr 2021
Viewed by 266
Abstract
Haemodialysis vascular access (VA) dysfunction is a major cause of morbidity in haemodialysis (HD) patients. Primary venous outflow occlusion and restenosis after percutaneous transluminal angioplasty (PTA) are two major obstacles for the long-term use of dialysis VA. It remains unclear whether oxidative stress [...] Read more.
Haemodialysis vascular access (VA) dysfunction is a major cause of morbidity in haemodialysis (HD) patients. Primary venous outflow occlusion and restenosis after percutaneous transluminal angioplasty (PTA) are two major obstacles for the long-term use of dialysis VA. It remains unclear whether oxidative stress markers can be used as predictors for thrombotic occlusion of VA and progressive stenosis dysfunction demanding PTA. All routine HD patients at one teaching hospital participated in this study including ankle-brachial index (ABI) examinations and serum oxidative stress markers. The serum oxidative stress markers (high-sensitivity C-reactive protein (hs-CRP), matrix metalloproteinase-2 (MMP-2), MMP-9, homocysteine, asymmetrical dimethylarginine (ADMA), nitrate oxidase (NO), tumour necrosis factor-α (TNF-α), monocyte chemotactic protein 1 (MCP-1), interleukin-1β (IL-1β), and transforming growth factor-β (TGF-β)) were measured using immunosorbent assays in 159 HD patients (83 men and 76 women; mean age: 65 ± 12 years). The participants met the following criteria: (1) received regular HD treatment for at least 6 months, without clinical evidence of acute or chronic inflammation, recent myocardial infarction, unstable angina or circulatory congestion; and (2) received an arteriovenous fistula (AVF)/arteriovenous graft (AVG: polytetrafluoroethylene, PTFE) as the current VA for more than 6 months, without interventions within the last 6 months. All the participants were followed up clinically for up to 12 months to estimate the amount of primary thrombotic occlusion and VA dysfunction demanding PTA. During the 12-month observation, 24 patients (15.1%) had primary thrombotic occlusion of VAs. Another 24 patients (15.1%) required PTA because of clinical dysfunction of access. Additionally, during the follow-up period, restenosis occurred in 12 patients (50% of 24 patients). The access types of arteriovenous grafts (AVGs) and a diagnosis of peripheral arterial occlusive disease (PAOD) were two strong predictors for acute thrombotic events of VA (hazard ratio (HR): 16.93 vs. 2.35; p < 0.001 vs. 0.047). Comparing dysfunctional with non-dysfunctional VAs, up to 27.7% of patients with high levels of ADMA (>0.6207 μM, N = 65) received required PTA compared with 4.4% of those with low levels (≤0.6207 μM; N = 90; p < 0.001). In multivariate analysis, the plasma baseline levels of ADMA independently conferred nearly 4.55 times the risk of primary stenotic dysfunction of HD VA (HR: 4.55; 95% confidence interval: 1.20 to 17.26; p = 0.026). In conclusion, our findings suggest the role of ADMA in the development of symptomatic VA dysfunction. Additionally, PAOD severity can be used in clinical practice to predict whether acute thrombotic occlusion of VA will easily occur in HD patients. Full article
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Open AccessArticle
NQO1 Deficiency Aggravates Renal Injury by Dysregulating Vps34/ATG14L Complex during Autophagy Initiation in Diabetic Nephropathy
Antioxidants 2021, 10(2), 333; https://doi.org/10.3390/antiox10020333 - 23 Feb 2021
Viewed by 599
Abstract
Diabetic nephropathy (DN) is one of the causes of end-stage renal failure, featuring renal fibrosis. However, autophagy, a vital process for intracellular homeostasis, can counteract renal fibrosis. Moreover, NAD(P)H: quinone dehydrogenase 1 (NQO1) modulates the ratios of reduced/oxidized nicotinamide nucleotides, exerting a cytoprotective [...] Read more.
Diabetic nephropathy (DN) is one of the causes of end-stage renal failure, featuring renal fibrosis. However, autophagy, a vital process for intracellular homeostasis, can counteract renal fibrosis. Moreover, NAD(P)H: quinone dehydrogenase 1 (NQO1) modulates the ratios of reduced/oxidized nicotinamide nucleotides, exerting a cytoprotective function. Here, to examine the role of NQO1 genes in DN progression, the levels of autophagy-related proteins and pro-fibrotic markers were assessed in silencing or overexpression of NQO1 in human proximal tubular cells (HK2), and C57BL/6 (wild-type) and Nqo1 knockout (KO) mice injected to streptozotocin (50 mg/kg). NQO1 deficiency impaired the autophagy process by suppressing basal expression of ClassⅢ PI 3-kinase (Vps34) and autophagy-related (ATG)14L and inducing the expressions of transforming growth factor beta (TGF-β1), Smad3, and matrix metallopeptidase9 (MMP9) in high-glucose (HG) -treated HK2 cells. Meanwhile, NQO1 overexpression increased the expression of Vps34 and ATG14L, while, reducing TGF-β1, Smad3 and MMP9 expression. In vivo, the expression of Vps34 and ATG14L were suppressed in Nqo1 KO mice indicating aggravated glomerular changes and interstitial fibrosis. Therefore, NQO1 deficiency dysregulated autophagy initiation in HK2 cells, with consequent worsened renal cell damage under HG condition. Moreover, STZ-treated Nqo1 KO mice showed that NQO1 deficiency aggravated renal fibrosis by dysregulating autophagy. Full article
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