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: 31 October 2024 | Viewed by 61

Special Issue Editor


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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Keywords

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

Published Papers

This special issue is now open for submission, see below for planned papers.

Planned Papers

The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.

Title: Dysfunction of mitochondrial dynamics induces endocytosis defect and cell damage in Drosophila nephrocytes
Authors: Jun-yi Zhu; Jianli Duan; Joyce van de Leemput; Zhe Han
Affiliation: University of Maryland School of Medicine
Abstract: Mitochondria are crucial for cellular ATP production. They are highly dynamic organelles, whose morphology and function are regulated 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 as a model to investigate the mitochondrial roles 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.

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