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Cells
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Drosophila Model in Molecular Mechanisms of Kidney Dysfunction
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Drosophila Model in Molecular Mechanisms of Kidney Dysfunction

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Tissues and Organs".

Deadline for manuscript submissions: closed (31 October 2024) | Viewed by 2920

Special Issue Editor

Dr. Junyi Zhu

E-Mail Website
Guest Editor
School of Medicine, University of Maryland, Baltimore, MD, USA
Interests: Drosophila; heart; kidney; congenital heart disease; nephrotic syndrome; genetic kidney diseases

Special Issue Information

Dear Colleagues,

Kidney dysfunction, resulting from various diseases, presents a significant global health challenge, affecting millions worldwide. The burden of this dysfunction is notably severe, given the high treatment costs and its profound impact on quality of life. Therefore, a deep understanding of the molecular mechanisms and the identification of potential drug targets are crucial for advancing research in kidney dysfunction.

In Drosophila, kidney and excretory functions are localized to the following three main tissues: the transporting renal (Malpighian) tubules, the reabsorptive hindgut, and the nephrocytes. This structural and functional similarity makes Drosophila an invaluable model for relating kidney phenotypes to human conditions.

In this Special Issue, we will apply Drosophila to explore the molecular mechanisms underlying kidney dysfunction; use Drosophila to model various kidney diseases, including nephrotic syndrome, diabetic nephropathy, and APOL1-associated kidney diseases; identify candidate genes for kidney diseases; investigate kidney development processes; and explore potential mechanisms for maintaining kidney function. 

Dr. Junyi Zhu
Guest Editor

Manuscript Submission Information

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Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 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

  • Drosophila
  • kidney dysfunction
  • disease processes
  • gene function
  • kidney development
  • signaling
  • cell biology

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Published Papers (2 papers)

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Research

17 pages, 11515 KiB  
Article
Actin Cytoskeleton and Integrin Components Are Interdependent for Slit Diaphragm Maintenance in Drosophila Nephrocytes
by Megan Delaney, Yunpo Zhao, Joyce van de Leemput, Hangnoh Lee and Zhe Han
Cells 2024, 13(16), 1350; https://doi.org/10.3390/cells13161350 - 14 Aug 2024
Cited by 2 | Viewed by 1344
Abstract
In nephrotic syndrome, the podocyte filtration structures are damaged in a process called foot process effacement. This is mediated by the actin cytoskeleton; however, which actins are involved and how they interact with other filtration components, like the basement membrane, remains poorly understood. [...] Read more.
In nephrotic syndrome, the podocyte filtration structures are damaged in a process called foot process effacement. This is mediated by the actin cytoskeleton; however, which actins are involved and how they interact with other filtration components, like the basement membrane, remains poorly understood. Here, we used the well-established Drosophila pericardial nephrocyte—the equivalent of podocytes in flies—knockdown models (RNAi) to study the interplay of the actin cytoskeleton (Act5C, Act57B, Act42A, and Act87E), alpha- and beta-integrin (basement membrane), and the slit diaphragm (Sns and Pyd). Knockdown of an actin gene led to variations of formation of actin stress fibers, the internalization of Sns, and a disrupted slit diaphragm cortical pattern. Notably, deficiency of Act5C, which resulted in complete absence of nephrocytes, could be partially mitigated by overexpressing Act42A or Act87E, suggesting at least partial functional redundancy. Integrin localized near the actin cytoskeleton as well as slit diaphragm components, but when the nephrocyte cytoskeleton or slit diaphragm was disrupted, this switched to colocalization, both at the surface and internalized in aggregates. Altogether, the data show that the interdependence of the slit diaphragm, actin cytoskeleton, and integrins is key to the structure and function of the Drosophila nephrocyte. Full article
(This article belongs to the Special Issue Drosophila Model in Molecular Mechanisms of Kidney Dysfunction)
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17 pages, 9325 KiB  
Article
Dysfunction of Mitochondrial Dynamics Induces Endocytosis Defect and Cell Damage in Drosophila Nephrocytes
by Jun-yi Zhu, Jianli Duan, Joyce van de Leemput and Zhe Han
Cells 2024, 13(15), 1253; https://doi.org/10.3390/cells13151253 - 25 Jul 2024
Cited by 1 | Viewed by 1130
Abstract
Mitochondria are crucial for cellular ATP production. They are highly dynamic organelles, whose morphology and function are controlled through mitochondrial fusion and fission. The specific roles of mitochondria in podocytes, the highly specialized cells of the kidney glomerulus, remain less understood. Given the [...] Read more.
Mitochondria are crucial for cellular ATP production. They are highly dynamic organelles, whose morphology and function are controlled through mitochondrial fusion and fission. The specific roles of mitochondria in podocytes, the highly specialized cells of the kidney glomerulus, remain less understood. Given the significant structural, functional, and molecular similarities between mammalian podocytes and Drosophila nephrocytes, we employed fly nephrocytes to explore the roles of mitochondria in cellular function. Our study revealed that alterations in the Pink1–Park (mammalian PINK1–PRKN) pathway can disrupt mitochondrial dynamics in Drosophila nephrocytes. This disruption led to either fragmented or enlarged mitochondria, both of which impaired mitochondrial function. The mitochondrial dysfunction subsequently triggered defective intracellular endocytosis, protein aggregation, and cellular damage. These findings underscore the critical roles of mitochondria in nephrocyte functionality. Full article
(This article belongs to the Special Issue Drosophila Model in Molecular Mechanisms of Kidney Dysfunction)
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