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Molecular Advances in Glomerular Diseases

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: 15 August 2024 | Viewed by 4092

Special Issue Editors

Division of Nephrology, Dialysis, and Transplantation, Scientific Institute for Research and Health Care (IRCCS), Istituto Giannina Gaslini, Largo Gaslini n 5, 16148 Genoa, Italy
Interests: glomerulonephritis; nephrotic syndrome genetics and mechanisms; therapy of nephrotic syndrome; systemic lupus erythematosus; lupus nephritis; mechanisms for autoimmunity
Renal Unit, Department of Medicine and Surgery, Università degli Studi di Milano Bicocca and ASST-Monza, 20900 Monza, Italy
Interests: autoimmunity clinical trials rheumatic diseases; cell adhesion renal rheumatoid arthritis; autoimmune disease autoantibodies clinical immunology
Division of Nephrology, Dialysis, Transplantation, IRCCS Istituto Giannina Gaslini, 16147 Genova, Italy
Interests: glomerular diseases

Special Issue Information

Dear Colleagues,

Glomerular diseases are a heterogeneous group of inflammatory diseases that represent an important cause of chronic morbidity, potentially evolving to renal failure. Pathology features, specific mechanisms causing glomerular damage, and association with extra-renal conditions represent the basis for a general classification that has clinical implications. Renal pathology varies from minimal lesions to diffuse glomerular proliferation, thickening of the basement membrane, and alteration of the microvasculature; circulating autoantibodies versus intrinsic or implanted antigens are often involved as a starting mechanism, and deposition of elements of the complement cascade may be involved as a main pathogenetic feature. Variable degrees of proteinuria, including nephrotic syndrome and hematuria, are the classical hallmarks that aggregate different conditions.

Evolutions in the pathogenesis of 'glomerular diseases' are sound and include the recognition of new autoantibodies causative of primary and secondary forms (Membranous nephropathy, Lupus nephritis), regulatory cells involved in inflammation, and other mechanisms of direct damage. Therapies do not witness those evolutions and have been substantially based, for many years, on the same drugs (steroids, CNI, mycophenolate mofetyl, anti-CD20).

Recognizing molecular factors would help us to implement potential targets of therapeutics, which is of particular interest in an era in which many new drugs targeting specific actors of inflammation, such as T/B cells, interleukins, intracellular factors, etc., have been developed and are already utilized with success in other inflammatory conditions. 

Dr. Gian Marco Ghiggeri
Dr. Renato Alberto Sinico
Dr. Andrea Angeletti
Guest Editors

Manuscript Submission Information

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Keywords

  • glomerulonephritis
  • proteinuria
  • autoantibodies

Published Papers (3 papers)

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Review

25 pages, 1472 KiB  
Review
Cytoskeleton Rearrangement in Podocytopathies: An Update
by Sijia Ma, Yang Qiu and Chun Zhang
Int. J. Mol. Sci. 2024, 25(1), 647; https://doi.org/10.3390/ijms25010647 - 04 Jan 2024
Viewed by 1057
Abstract
Podocyte injury can disrupt the glomerular filtration barrier (GFB), leading to podocytopathies that emphasize podocytes as the glomerulus’s key organizer. The coordinated cytoskeleton is essential for supporting the elegant structure and complete functions of podocytes. Therefore, cytoskeleton rearrangement is closely related to the [...] Read more.
Podocyte injury can disrupt the glomerular filtration barrier (GFB), leading to podocytopathies that emphasize podocytes as the glomerulus’s key organizer. The coordinated cytoskeleton is essential for supporting the elegant structure and complete functions of podocytes. Therefore, cytoskeleton rearrangement is closely related to the pathogenesis of podocytopathies. In podocytopathies, the rearrangement of the cytoskeleton refers to significant alterations in a string of slit diaphragm (SD) and focal adhesion proteins such as the signaling node nephrin, calcium influx via transient receptor potential channel 6 (TRPC6), and regulation of the Rho family, eventually leading to the disorganization of the original cytoskeletal architecture. Thus, it is imperative to focus on these proteins and signaling pathways to probe the cytoskeleton rearrangement in podocytopathies. In this review, we describe podocytopathies and the podocyte cytoskeleton, then discuss the molecular mechanisms involved in cytoskeleton rearrangement in podocytopathies and summarize the effects of currently existing drugs on regulating the podocyte cytoskeleton. Full article
(This article belongs to the Special Issue Molecular Advances in Glomerular Diseases)
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13 pages, 304 KiB  
Review
Extracellular Vesicles as Source of Biomarkers in Glomerulonephritis
by Maurizio Bruschi, Giovanni Candiano, Andrea Angeletti, Francesca Lugani and Isabella Panfoli
Int. J. Mol. Sci. 2023, 24(18), 13894; https://doi.org/10.3390/ijms241813894 - 09 Sep 2023
Cited by 2 | Viewed by 915
Abstract
Kidney disease is a global health and healthcare burden. Glomerulonephritis (Gn), both primary and secondary, is generally characterized by an inflammatory glomerular injury and may lead to end-stage renal disease. Kidney biopsy is fundamental to the diagnosis; however, kidney biopsy presents some concerns [...] Read more.
Kidney disease is a global health and healthcare burden. Glomerulonephritis (Gn), both primary and secondary, is generally characterized by an inflammatory glomerular injury and may lead to end-stage renal disease. Kidney biopsy is fundamental to the diagnosis; however, kidney biopsy presents some concerns that may partly hamper the clinical process. Therefore, more accurate diagnostic tools are needed. Extracellular vesicles (EVs) are membranous vesicles released by cells and found in bodily fluids, including urine. EVs mediate intercellular signaling both in health and disease. EVs can have both harmful and cytoprotective effects in kidney diseases, especially Gn. Previous findings reported that the specific cargo of urinary EV contains an aerobic metabolic ability that may either restore the recipient cell metabolism or cause oxidative stress production. Here, we provide an overview of the most recent proteomic findings on the role of EVs in several aspects of glomerulopathies, with a focus on this metabolic and redox potential. Future studies may elucidate how the ability of EVs to interfere with aerobic metabolism and redox status can shed light on aspects of Gn etiology which have remained elusive so far. Full article
(This article belongs to the Special Issue Molecular Advances in Glomerular Diseases)
12 pages, 1253 KiB  
Review
Mechanisms Limiting Renal Tissue Protection and Repair in Glomerulonephritis
by Andrea Angeletti, Maurizio Bruschi, Xuliana Kajana, Sonia Spinelli, Enrico Verrina, Francesca Lugani, Gialuca Caridi, Corrado Murtas, Giovanni Candiano, Marco Prunotto and Gian Marco Ghiggeri
Int. J. Mol. Sci. 2023, 24(9), 8318; https://doi.org/10.3390/ijms24098318 - 05 May 2023
Cited by 5 | Viewed by 1576
Abstract
Glomerulonephritis are renal disorders resulting from different pathogenic mechanisms (i.e., autoimmunity, complement, inflammatory activation, etc.). Clarifying details of the pathogenic cascade is basic to limit the progression from starting inflammation to degenerative stages. The balance between tissue injury, activation of protective systems and [...] Read more.
Glomerulonephritis are renal disorders resulting from different pathogenic mechanisms (i.e., autoimmunity, complement, inflammatory activation, etc.). Clarifying details of the pathogenic cascade is basic to limit the progression from starting inflammation to degenerative stages. The balance between tissue injury, activation of protective systems and renal tissue repair determines the final outcome. Induction of an oxidative stress is part of glomerular inflammation and activation of protective antioxidant systems has a crucial role in reducing tissue effects. The generation of highly reactive oxygen species can be evaluated in vivo by tracing the inner-layer content of phosphatidyl ethanolamine and phosphatidyl serine in cell membranes. Albumin is the major antioxidant in serum and the level of oxidized albumin is another indirect sign of oxidative stress. Studies performed in Gn, specifically in FSGS, showed a high degree of oxidation in most contexts. High levels of circulating anti-SOD2 antibodies, limiting the detoxyfing activity of SOD2, have been detected in autoimmune Gn(lupus nephritis and membranous nephropathy) in association with persistence of proteinuria and worsening of renal function. In renal transplant, high levels of circulating anti-Glutathione S-transferase antibodies have been correlated with chronic antibody rejection and progressive loss of renal function. Annexins, mainly ANXA1 and ANXA2, play a general anti-inflammatory effect by inhibiting neutrophil functions. Cytosolic ANXA1 is decreased in apoptotic neutrophils of patients with glomerular polyangitis in association with delayed apoptosis that is considered the mechanism for polyangitis. High circulating levels of anti-ANXA1 and anti-ANXA2 antibodies characterize lupus nephritis implying a reduced anti-inflammatory effect. High circulating levels of antibodies targeting Macrophages (anti-FMNL1) have been detected in Gn in association with proteinuria. They potentially modify the intra-glomerular presence of protective macrophages (M2a, M2c) thus acting on the composition of renal infiltrate and on tissue repair. Full article
(This article belongs to the Special Issue Molecular Advances in Glomerular Diseases)
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