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Special Issue "Kidney Inflammation, Injury and Regeneration 2020"

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: 31 August 2020.

Special Issue Editors

Prof. Dr. Patrick C. Baer
Website1 Website2
Guest Editor
Universitätsklinikum FrankfurtZentrum der Inneren Medizin - NephrologieTheodor-Stern-Kai 7 D-60590 Frankfurt
Interests: acute kidney injury; renal tubular cells; in vitro models; in vivo models; kidney regeneration; epithelial cells; mesenchymal stem cells; adipose-derived stromal/stem cells; cell differentiation; extracellular vesicles
Special Issues and Collections in MDPI journals
Dr. Benjamin Koch
Website
Guest Editor
Nephrology, Department of Internal Medicine, Goethe-Universitat Frankfurt am Main, Frankfurt am Main, Germany
Interests: transcriptomics in acute and chronic kidney injury; novel blood filtration devices in viral and bacterial sepsis; in vitro models of viral and bacterial sepsis; donor-specific antibodies in renal transplantation; extracellular vesicles; renal regeneration
Special Issues and Collections in MDPI journals
Prof. Dr. Helmut Geiger
Website
Guest Editor
Nephrology, Department of Internal Medicine, Goethe-Universitat Frankfurt am Main, Frankfurt am Main, Germany
Interests: renal diseases; acute kidney injury; chronic kidney; hypertension; dialysis; renal transplantation; renal regeneration
Special Issues and Collections in MDPI journals

Special Issue Information

Dear Colleagues,

Acute kidney injury (AKI) is still associated with high morbidity and mortality incidence rates, and also bears an elevated risk of chronic kidney disease in the sequel. Whereas the kidney has a remarkable capacity for regeneration after injury and may recover completely depending on the type of renal lesions, the options for clinical intervention are restricted to fluid management and extracorporeal kidney support. The development of novel therapies to prevent AKI, to improve renal regeneration capacity after AKI, and to preserve renal function—in both the short- and long-term—is urgently needed.

This Special Issue will include papers investigating the pathological mechanisms of renal inflammation and AKI, and diagnostics using new biomarkers. Furthermore, experimental in vitro and in vivo studies and clinical studies examining potential new approaches to attenuate kidney dysfunction are welcome.

This Special Issue welcomes original research and review papers. Potential topics include, but are not limited to, the following:

  1. Molecular mechanisms of kidney inflammation and epithelial cell injury;
  2. Acute kidney injury (AKI)—Pathological mechanisms and new biomarkers;
  3. Kidney inflammation and injury: Transcriptomics and proteomics;
  4. In vitro models simulating tubular inflammation, injury, and regeneration;
  5. In vivo AKI models;
  6. Investigations to preserve renal function using stem cells or their derivates.
Prof. Dr. Patrick C. Baer
Dr. Benjamin Koch
Prof. Dr. Helmut Geiger
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 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

  • renal inflammation
  • acute kidney injury
  • chronic kidney injury
  • pathological mechanisms
  • tubular epithelial cells
  • epithelial recovery
  • biomarkers
  • transcriptomics and proteomics
  • urinary extracellular vesicles
  • epithelial recovery
  • organ regeneration
  • tissue engineering
  • regenerative medicine

Related Special Issue

Published Papers (4 papers)

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Research

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Open AccessArticle
Cyclophilin A Promotes Inflammation in Acute Kidney Injury but Not in Renal Fibrosis
Int. J. Mol. Sci. 2020, 21(10), 3667; https://doi.org/10.3390/ijms21103667 - 22 May 2020
Abstract
Cyclophilin A (CypA) is a highly abundant protein in the cytoplasm of most mammalian cells. Beyond its homeostatic role in protein folding, CypA is a Damage-Associated Molecular Pattern which can promote inflammation during tissue injury. However, the role of CypA in kidney disease [...] Read more.
Cyclophilin A (CypA) is a highly abundant protein in the cytoplasm of most mammalian cells. Beyond its homeostatic role in protein folding, CypA is a Damage-Associated Molecular Pattern which can promote inflammation during tissue injury. However, the role of CypA in kidney disease is largely unknown. This study investigates the contribution of CypA in two different types of kidney injury: acute tubular necrosis and progressive interstitial fibrosis. CypA (Ppia) gene deficient and wild type (WT) littermate controls underwent bilateral renal ischaemia/reperfusion injury (IRI) and were killed 24 h later or underwent left unilateral ureteric obstruction (UUO) and were killed 7 days later. In the IRI model, CypA−/− mice showed substantial protection against the loss of renal function and from tubular cell damage and death. This was attributed to a significant reduction in neutrophil and macrophage infiltration since CypA−/− tubular cells were not protected from oxidant-induced cell death in vitro. In the UUO model, CypA−/− mice were not protected from leukocyte infiltration or renal interstitial fibrosis. In conclusion, CypA promotes inflammation and acute kidney injury in renal IRI, but does not contribute to inflammation or interstitial fibrosis in a model of progressive kidney fibrosis. Full article
(This article belongs to the Special Issue Kidney Inflammation, Injury and Regeneration 2020)
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Open AccessArticle
Cilastatin Preconditioning Attenuates Renal Ischemia-Reperfusion Injury via Hypoxia Inducible Factor-1α Activation
Int. J. Mol. Sci. 2020, 21(10), 3583; https://doi.org/10.3390/ijms21103583 - 19 May 2020
Abstract
Cilastatin is a specific inhibitor of renal dehydrodipeptidase-1. We investigated whether cilastatin preconditioning attenuates renal ischemia-reperfusion (IR) injury via hypoxia inducible factor-1α (HIF-1α) activation. Human proximal tubular cell line (HK-2) was exposed to ischemia, and male C57BL/6 mice were subjected to bilateral kidney [...] Read more.
Cilastatin is a specific inhibitor of renal dehydrodipeptidase-1. We investigated whether cilastatin preconditioning attenuates renal ischemia-reperfusion (IR) injury via hypoxia inducible factor-1α (HIF-1α) activation. Human proximal tubular cell line (HK-2) was exposed to ischemia, and male C57BL/6 mice were subjected to bilateral kidney ischemia and reperfusion. The effects of cilastatin preconditioning were investigated both in vitro and in vivo. In HK-2 cells, cilastatin upregulated HIF-1α expression in a time- and dose-dependent manner. Cilastatin enhanced HIF-1α translation via the phosphorylation of Akt and mTOR was followed by the upregulation of erythropoietin (EPO) and vascular endothelial growth factor (VEGF). Cilastatin did not affect the expressions of PHD and VHL. However, HIF-1α ubiquitination was significantly decreased after cilastatin treatment. Cilastatin prevented the IR-induced cell death. These cilastatin effects were reversed by co-treatment of HIF-1α inhibitor or HIF-1α small interfering RNA. Similarly, HIF-1α expression and its upstream and downstream signaling were significantly enhanced in cilastatin-treated kidney. In mouse kidney with IR injury, cilastatin treatment decreased HIF-1α ubiquitination independent of PHD and VHL expression. Serum creatinine level and tubular necrosis, and apoptosis were reduced in cilastatin-treated kidney with IR injury, and co-treatment of cilastatin with an HIF-1α inhibitor reversed these effects. Thus, cilastatin preconditioning attenuated renal IR injury via HIF-1α activation. Full article
(This article belongs to the Special Issue Kidney Inflammation, Injury and Regeneration 2020)
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Open AccessArticle
Macrophage-Secreted Lipocalin-2 Promotes Regeneration of Injured Primary Murine Renal Tubular Epithelial Cells
Int. J. Mol. Sci. 2020, 21(6), 2038; https://doi.org/10.3390/ijms21062038 - 16 Mar 2020
Abstract
Lipocalin-2 (Lcn-2) is rapidly upregulated in macrophages after renal tubular injury and acts as renoprotective and pro-regenerative agent. Lcn-2 possesses the ability to bind and transport iron with high affinity. Therefore, the present study focuses on the decisive role of the Lcn-2 iron-load [...] Read more.
Lipocalin-2 (Lcn-2) is rapidly upregulated in macrophages after renal tubular injury and acts as renoprotective and pro-regenerative agent. Lcn-2 possesses the ability to bind and transport iron with high affinity. Therefore, the present study focuses on the decisive role of the Lcn-2 iron-load for its pro-regenerative function. Primary mouse tubular epithelial cells were isolated from kidney tissue of wildtype mice and incubated with 5 µM Cisplatin for 24 h to induce injury. Bone marrow-derived macrophages of wildtype and Lcn-2−/− mice were isolated and polarized with IL-10 towards an anti-inflammatory, iron-release phenotype. Their supernatants as well as recombinant iron-loaded holo-Lcn-2 was used for stimulation of Cisplatin-injured tubular epithelial cells. Incubation of tubular epithelial cells with wildtype supernatants resulted in less damage and induced cellular proliferation, whereas in absence of Lcn-2 no protective effect was observed. Epithelial integrity as well as cellular proliferation showed a clear protection upon rescue experiments applying holo-Lcn-2. Notably, we detected a positive correlation between total iron amounts in tubular epithelial cells and cellular proliferation, which, in turn, reinforced the assumed link between availability of Lcn-2-bound iron and recovery. We hypothesize that macrophage-released Lcn-2-bound iron is provided to tubular epithelial cells during toxic cell damage, whereby injury is limited and recovery is favored. Full article
(This article belongs to the Special Issue Kidney Inflammation, Injury and Regeneration 2020)
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Review

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Open AccessReview
The Influence of Inflammation on Anemia in CKD Patients
Int. J. Mol. Sci. 2020, 21(3), 725; https://doi.org/10.3390/ijms21030725 - 22 Jan 2020
Abstract
Anemia is frequently observed in the course of chronic kidney disease (CKD) and it is associated with diminishing the quality of a patient’s life. It also enhances morbidity and mortality and hastens the CKD progression rate. Patients with CKD frequently suffer from a [...] Read more.
Anemia is frequently observed in the course of chronic kidney disease (CKD) and it is associated with diminishing the quality of a patient’s life. It also enhances morbidity and mortality and hastens the CKD progression rate. Patients with CKD frequently suffer from a chronic inflammatory state which is related to a vast range of underlying factors. The results of studies have demonstrated that persistent inflammation may contribute to the variability in Hb levels and hyporesponsiveness to erythropoietin stimulating agents (ESA), which are frequently observed in CKD patients. The understanding of the impact of inflammatory cytokines on erythropoietin production and hepcidin synthesis will enable one to unravel the net of interactions of multiple factors involved in the pathogenesis of the anemia of chronic disease. It seems that anti-cytokine and anti-oxidative treatment strategies may be the future of pharmacological interventions aiming at the treatment of inflammation-associated hyporesponsiveness to ESA. The discovery of new therapeutic approaches towards the treatment of anemia in CKD patients has become highly awaited. The treatment of anemia with erythropoietin (EPO) was associated with great benefits for some patients but not all. Full article
(This article belongs to the Special Issue Kidney Inflammation, Injury and Regeneration 2020)
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