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Advanced Molecular Insights into Renal Disorders

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (31 March 2024) | Viewed by 17445

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Special Issue Editor

Dr. Keiko Hosohata

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Guest Editor

Education and Research Center for Clinical Pharmacy, Osaka University of Pharmaceutical Sciences, 4-20-1 Nasahara, Takatsuki 569-1094, Japan
Interests: inflammation; reactive oxygen species; renal physiology; blood pressure regulation; biomarker; clinical pharmacology; toxicology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Oxidative stress is involved in the development of renal disease as well as cardiovascular disease, diabetes, and cerebral disease, and cancers. The complex crosstalk of oxidative status with inflammation, cell death, EMT (epithelial-mesenchymal transition) are still far from being completely understood, since reciprocal and opposite influences can be exerted between these pathogenic factors. In addition, various nuclear factors and receptors involved in the regulation of antioxidant defense, nitric oxide production, inflammation, energy, and/or iron metabolism provide new targets for the prevention and treatment of renal disease and comorbid diseases.

Recent studies have demonstrated that natural antioxidants can modulate oxidative stress and improve immune function. Thus, the role of compounds with antioxidant properties that promote health and counteract oxidative stress in the renal disease is worth investigating further. An exhaustive understanding of the role of the involvement of antioxidants in redox modulation would be useful for potential interventions and, subsequently, promoting health.

Therefore, we aim to publish a Special Issue which can cover a wide spectrum, from biological to translational studies, in the field of renal disorders.

This Special Issue will gather reviews and original data that focus on defining the following:

Abnormalities in the antioxidant system in patients with renal diseases;
Antioxidant therapeutics;
Biomarkers and diagnostic methods in oxidative stress.

Dr. Keiko Hosohata
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 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

reactive oxygen species (ROS)
inflammation
metabolic syndrome
antioxidant response
redox balance
aging
proinflammatory signals
kidney

Published Papers (7 papers)

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Research

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16 pages, 10512 KiB

Open AccessArticle

Sex-Specific Effects of Estradiol and Progesterone in Ischemic Kidney Injury

by Nadezda V. Andrianova, Anna A. Brezgunova, Marina I. Buyan, Ciara I. Makievskaya, Andrey I. Buyan, Kseniia S. Cherkesova, Irina B. Pevzner, Ljubava D. Zorova, Dmitry B. Zorov, Egor Y. Plotnikov and Vasily A. Popkov

Int. J. Mol. Sci. 2024, 25(6), 3155; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms25063155 - 09 Mar 2024

Viewed by 2193

Abstract

The positive effects of female sex hormones, particularly estradiol and progesterone, have been observed in treatment of various pathologies. Acute kidney injury (AKI) is a common condition in hospitalized patients in which the molecular mechanisms of hormone action are poorly characterized. In this study, we investigated the influence of estradiol and progesterone on renal cells during ischemic injury. We performed both in vivo experiments on female and male rats and in vitro experiments on renal tubular cells (RTCs) obtained from the kidneys of intact animals of different sexes. Since mitochondria play an important role in the pathogenesis of AKI, we analyzed the properties of individual mitochondria in renal cells, including the area, roundness, mitochondrial membrane potential, and mitochondrial permeability transition pore (mPTP) opening time. We found that pre-treatment with progesterone or estradiol attenuated the severity of ischemia/reperfusion (I/R)-induced AKI in female rats, whereas in male rats, these hormones exacerbated renal dysfunction. We demonstrated that the mPTP opening time was higher in RTCs from female rats than that in those from male rats, which may be one of the reasons for the higher tolerance of females to ischemic injury. In RTCs from the kidneys of male rats, progesterone caused mitochondrial fragmentation, which can be associated with reduced cell viability. Thus, therapy with progesterone or estradiol displays quite different effects depending on sex, and could be only effective against ischemic AKI in females. Full article

(This article belongs to the Special Issue Advanced Molecular Insights into Renal Disorders)

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12 pages, 8768 KiB

Open AccessArticle

Role of Transcription Factor EB in Mitochondrial Dysfunction of Cisplatin-Induced Acute Kidney Injury

by Shujun Wang, Yanse Chen, Hongluan Wu, Xiaoyu Li, Haiyan Xiao, Qingjun Pan and Hua-Feng Liu

Int. J. Mol. Sci. 2023, 24(3), 3028; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms24033028 - 03 Feb 2023

Cited by 1 | Viewed by 1597

Abstract

Cisplatin, a widely used anticancer agent, can cause nephrotoxicity, including both acute kidney injury (AKI) and chronic kidney diseases, by accumulating in renal tubular epithelial cells (TECs). Mitochondrial pathology plays an important role in the pathogenesis of AKI. Based on the regulatory role of transcription factor EB (TFEB) in mitochondria, we investigated whether TFEB is involved in cisplatin-induced TEC damage. The results show that the expression of TFEB decreased in a concentration-dependent manner in both mouse kidney tissue and HK-2 cells when treated with cisplatin. A knockdown of TFEB aggravated cisplatin-induced renal TEC injury, which was partially reversed by TFEB overexpression in HK-2 cells. It was further observed that the TFEB knockdown also exacerbated cisplatin-induced mitochondrial damage in vitro, and included the depolarization of membrane potential, mitochondrial fragmentation and swelling, and the production of reactive oxygen species. In contrast, TFEB overexpression alleviated cisplatin-induced mitochondrial damage in TECs. These findings suggest that decreased TFEB expression may be a key mechanism of mitochondrial dysfunction in cisplatin-induced AKI, and that upregulation of TFEB has the potential to act as a therapeutic target to alleviate mitochondrial dysfunction and cisplatin-induced TEC injury. This study is important for developing therapeutic strategies to manipulate mitochondria through TFEB to delay AKI progression. Full article

(This article belongs to the Special Issue Advanced Molecular Insights into Renal Disorders)

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17 pages, 7474 KiB

Open AccessArticle

Process of Glucose Increases Rather Than Constant High Glucose Was the Main Cause of Abnormal Glucose Induced Glomerulus Epithelial Cells Inflammatory Response

by Jiancheng Qi, Weiyu Liu, Linli Gan, Hongrui Guo, Yue Xie, Liping Gou, Dongjie Cai, Jizong Zhang, Junliang Deng, Zhihua Ren, Jing Fang and Zhicai Zuo

Int. J. Mol. Sci. 2023, 24(1), 600; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms24010600 - 29 Dec 2022

Cited by 4 | Viewed by 1215

Abstract

Abnormal glycemia is frequently along with nephritis, whose pathogenesis is unexplicit. Here, we investigated the effects of abnormal glucose on the renal glomerulus epithelial cells by stimulating immortalized bovine renal glomerulus epithelial (MDBK) cells with five different levels of glucose, including low glucose (2.5 mM for 48 h, LG), normal glucose (5 mM for 48 h, NG), high glucose (25 mM for 48 h, HG), increasing glucose (24 h of 2.5 mM glucose followed by 24 h of 25 mM, IG), and reducing glucose (24 h of 25 mM glucose followed by 24 h of 2.5 mM, RG). The results showed that LG and RG treatments had nonsignificant effects (p > 0.05) on the viability of MDBK cells. HG treatment decreased the viabilities of cells (p < 0.01) without triggering an apparent inflammatory response by activating the nox4/ROS/p53/caspase-3-mediated apoptosis pathway. IG treatment decreased the viabilities of cells significantly (p < 0.01) with high levels of pro-inflammatory cytokines IL-1β and IL-18 in the supernatant (p < 0.05) by triggering the txnip/nlrp3/gsdmd-mediated pyroptosis pathway. These results indicated that the process of glucose increase rather than the constant high glucose was the main cause of abnormal glucose-induced MDBK cell inflammatory death, prompting that the process of glycemia increases might be mainly responsible for the nephritis in diabetic nephropathy, underlining the importance of glycemic control in diabetes patients. Full article

(This article belongs to the Special Issue Advanced Molecular Insights into Renal Disorders)

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19 pages, 6931 KiB

Open AccessArticle

Methotrexate-Induced Alteration of Renal Aquaporins 1 and 2, Oxidative Stress and Tubular Apoptosis Can Be Attenuated by Omega-3 Fatty Acids Supplementation

by Mosaab Salah El-din El-Agawy, Alaa Mohamed Mohamed Badawy, Mohammed R. Rabei, Mohamed Mahmoud Abdelraheem Elshaer, Eman Mohamad El Nashar, Mansour A. Alghamdi, Mohammed A. Alshehri and Hassan Reda Hassan Elsayed

Int. J. Mol. Sci. 2022, 23(21), 12794; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms232112794 - 24 Oct 2022

Cited by 8 | Viewed by 2203

Abstract

Methotrexate (MTX) is a potent anti-cancer drug, commonly associated with nephrotoxicity via the induction of oxidative stress and apoptosis with alteration of renal water channel proteins, namely aquaporins (AQPs). Omega-3 long-chain polyunsaturated fatty acids (LC-PUFA) have shown cytoprotective effects through their anti-oxidant and antiapoptotic activities. The present study aims for the first time to explore the role of LC-PUFA against MTX-induced nephrotoxicity. Rats were divided into the following groups: saline control, LC-PUFA control, MTX, MTX + LC-PUFA (150 mg/kg), or MTX + LC-PUFA (300 mg/kg). Then, H&E staining and immunohistochemical staining for the anti-apoptosis marker B-cell lymphoma 2 (BCL-2), the apoptosis marker BCL2-Associated X Protein (BAX), the proinflammatory marker Nuclear factor kappa B (NF-kB), AQPs 1 and 2 were performed in kidney sections with an assessment of renal oxidative stress. The MTX caused a renal histopathological alteration, upregulated renal BAX and NF-kB, downregulated Bcl-2 and AQP1, altered the distribution of AQP2, and caused oxidative stress. The LC-PUFA attenuated the pathological changes and decreased renal BAX and NF-kB, increased BCL-2 and AQP1, restored the normal distribution of AQP2, and decreased the oxidative stress. Therefore, LC-PUFA is a good adjuvant to MTX to prevent its adverse effects on kidneys through its antiapoptotic, antioxidant, and anti-inflammatory effect and its role in the restoration of the expression of AQPs 1 and 2. Full article

(This article belongs to the Special Issue Advanced Molecular Insights into Renal Disorders)

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Review

Jump to: Research

16 pages, 1519 KiB

Open AccessReview

Urinary L-FABP as an Early Biomarker for Pediatric Acute Kidney Injury Following Cardiac Surgery with Cardiopulmonary Bypass: A Systematic Review and Meta-Analysis

by Bruno Wilnes, Beatriz Castello-Branco, Bárbara Castello Branco, André Sanglard, Pedro Alves Soares Vaz de Castro and Ana Cristina Simões-e-Silva

Int. J. Mol. Sci. 2024, 25(9), 4912; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms25094912 - 30 Apr 2024

Viewed by 154

Abstract

Acute kidney injury (AKI) following surgery with cardiopulmonary bypass (CPB-AKI) is common in pediatrics. Urinary liver-type fatty acid binding protein (uL-FABP) increases in some kidney diseases and may indicate CPB-AKI earlier than current methods. The aim of this systematic review with meta-analysis was to evaluate the potential role of uL-FABP in the early diagnosis and prediction of CPB-AKI. Databases Pubmed/MEDLINE, Scopus, and Web of Science were searched on 12 November 2023, using the MeSH terms “Children”, “CPB”, “L-FABP”, and “Acute Kidney Injury”. Included papers were revised. AUC values from similar studies were pooled by meta-analysis, performed using random- and fixed-effect models, with p < 0.05. Of 508 studies assessed, nine were included, comprising 1658 children, of whom 561 (33.8%) developed CPB-AKI. Significantly higher uL-FABP levels in AKI versus non-AKI patients first manifested at baseline to 6 h post-CPB. At 6 h, uL-FABP correlated with CPB duration (r = 0.498, p = 0.036), postoperative serum creatinine (r = 0.567, p < 0.010), and length of hospital stay (r = 0.722, p < 0.0001). Importantly, uL-FABP at baseline (AUC = 0.77, 95% CI: 0.64–0.89, n = 365), 2 h (AUC = 0.71, 95% CI: 0.52–0.90, n = 509), and 6 h (AUC = 0.76, 95% CI: 0.72–0.80, n = 509) diagnosed CPB-AKI earlier. Hence, higher uL-FABP levels associate with worse clinical parameters and may diagnose and predict CPB-AKI earlier. Full article

(This article belongs to the Special Issue Advanced Molecular Insights into Renal Disorders)

15 pages, 672 KiB

Open AccessReview

Diet and Proteinuria: State of Art

by Paolo Ria, Antonio De Pascalis, Anna Zito, Silvia Barbarini, Marcello Napoli, Antonietta Gigante and Gian Pio Sorice

Int. J. Mol. Sci. 2023, 24(1), 44; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms24010044 - 20 Dec 2022

Cited by 4 | Viewed by 4991

Abstract

Proteinuria is a broad term used to describe the pathological presence of proteins, including albumin, globulin, Bence-Jones protein, and mucoprotein in the urine. When persistent, proteinuria is a marker of kidney damage and represents a reliable predictor of the risk of progression of renal failure. Medical nutrition therapy is imperative for patients with proteinuria because it may slow the progression of renal disease. The aim of this review is to explore different nutritional approaches in the management of proteinuria and their influence on pathophysiological processes. As such, protein restriction is the main dietary intervention. Indeed, other management approaches are frequently used to reduce it regarding micro and macronutrients, but also the dietary style. Among these, the nutritional approach represents one of the most used and controversial interventions and the studies rarely take the form of randomized and controlled trials. With this work we aspire to analyze current clinical knowledge of how nutrition could influence proteinuria, potentially representing a useful tool in the management of proteinuric nephropathy. Full article

(This article belongs to the Special Issue Advanced Molecular Insights into Renal Disorders)

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11 pages, 1302 KiB

Open AccessReview

Ferroptosis: A Potential Therapeutic Target in Acute Kidney Injury

by Keiko Hosohata, Tanisorn Harnsirikarn and Susama Chokesuwattanaskul

Int. J. Mol. Sci. 2022, 23(12), 6583; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23126583 - 13 Jun 2022

Cited by 26 | Viewed by 4189

Abstract

Ferroptosis is a recently recognized form of nonapoptotic cell death that is triggered by reactive oxidative species (ROS) due to iron overload, lipid peroxidation accumulation, or the inhibition of phospholipid hydroperoxidase glutathione peroxidase 4 (GPX4). Recent studies have reported that ferroptosis plays a vital role in the pathophysiological process of multiple systems such as the nervous, renal, and pulmonary systems. In particular, the kidney has higher rates of O₂ consumption in its mitochondria than other organs; therefore, it is susceptible to imbalances between ROS and antioxidants. In ischemia/reperfusion (I/R) injury, which is damage caused by the restoring blood flow to ischemic tissues, the release of ROS and reactive nitrogen species is accelerated and contributes to subsequent inflammation and cell death, such as ferroptosis, as well as apoptosis and necrosis being induced. At the same time, I/R injury is one of the major causes of acute kidney injury (AKI), causing significant morbidity and mortality. This review highlights the current knowledge on the involvement of ferroptosis in AKI via oxidative stress. Full article

(This article belongs to the Special Issue Advanced Molecular Insights into Renal Disorders)

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