Developmental Biology of the Kidney: From Molecular Mechanisms to Congenital Disorders

A special issue of Journal of Developmental Biology (ISSN 2221-3759).

Deadline for manuscript submissions: closed (31 January 2026) | Viewed by 1060

Special Issue Editors


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Guest Editor
1. Department of Anatomy, Histology and Embryology, University of Split School of Medicine, Šoltanska 2A, 21000 Split, Croatia
2. Center for Translational Research in Biomedicine, University of Split School of Medicine, Soltanska 2A, 21000 Split, Croatia
Interests: kidney development; congenital anomalies of the kidney; next-generation sequencing; chronic kidney diseases; precision medicine; diabetic nephropathy
Special Issues, Collections and Topics in MDPI journals

E-Mail Website
Guest Editor
1. Department of Anatomy, Histology and Embryology, University of Split School of Medicine, Šoltanska 2A, 21000 Split, Croatia
2. Center for Translational Research in Biomedicine, University of Split School of Medicine, Šoltanska 2A, 21000 Split, Croatia
Interests: kidney; kidney development; mouse knockout models; kidney diseases; CAKUT
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

We are pleased to announce a Special Issue entitled “Developmental Biology of the Kidney: From Molecular Mechanisms to Congenital Disorders”, which is to be published in The Journal of Developmental Biology. This Special Issue will focus on uncovering the developmental processes and molecular mechanisms that shape kidney formation and their implications for congenital and acquired renal disorders.

Kidney development is a complex and tightly regulated process involving intricate cellular signaling networks, genetic and epigenetic programming, and organogenesis pathways. The dysregulation of these processes can lead to congenital anomalies of the kidney and urinary tract (CAKUT) and other developmental disorders with lifelong health consequences. Advancing our understanding of these mechanisms is critical to identifying therapeutic targets and improving outcomes for individuals affected by such conditions.

We welcome original research articles, reviews, and perspectives addressing the following topics, among others:

  • Mechanisms of nephrogenesis and kidney organogenesis.
  • Genetic and epigenetic regulation during kidney development.
  • Developmental origins of kidney diseases, including CAKUT.
  • Insights from animal models and next-generation sequencing in kidney development.
  • Role of signaling pathways and transcriptional networks in renal development.
  • Advances in regenerative medicine and kidney tissue engineering.

This Special Issue provides an excellent platform to share your latest findings with the developmental biology community and contribute to advancing knowledge in this critical field.

You may choose our Joint Special Issue in Biomolecules.

Prof. Dr. Katarina Vukojević
Dr. Anita Racetin
Guest Editors

Manuscript Submission Information

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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. Journal of Developmental Biology is an international peer-reviewed open access quarterly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1800 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

  • kidney development
  • renal physiology
  • kidney disease
  • molecular mechanisms
  • cellular signaling
  • gene expression
  • biomarkers
  • renal pathophysiology
  • therapeutic targets

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Published Papers (1 paper)

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Research

11 pages, 2258 KB  
Article
Influence of Obstructive Uropathy on Cyst Formation and Nephrogenesis: Insights from a Fetal Lamb Model
by Kohei Kawaguchi, Takuya Kawaguchi, Juma Obayashi, Yasuji Seki, Kunihide Tanaka, Kei Ohyama, Junki Koike, Shigeyuki Furuta, Kevin C. Pringle and Hiroaki Kitagawa
J. Dev. Biol. 2026, 14(1), 5; https://doi.org/10.3390/jdb14010005 - 9 Jan 2026
Viewed by 431
Abstract
Obstructive uropathy (OU) during fetal development induces a fetal cystic dysplastic kidney. The mechanisms of cyst formation and the onset of renal dysfunction remain unclear. Determining whether nephrogenic potential persists during fetal life may suggest whether early intervention could preserve renal development. We [...] Read more.
Obstructive uropathy (OU) during fetal development induces a fetal cystic dysplastic kidney. The mechanisms of cyst formation and the onset of renal dysfunction remain unclear. Determining whether nephrogenic potential persists during fetal life may suggest whether early intervention could preserve renal development. We aimed to evaluate residual nephrogenic activity in fetal cystic dysplastic kidneys using β-catenin and CD10 immunostaining, and to assess whether the site of obstruction influences cystogenesis. After appropriate approval, 20 timed-gestation fetal lambs had OU created at 60 days. Males underwent urethral and urachal ligation (n = 8, 3 lost), and females underwent unilateral ureteric ligation (n = 8, 1 lost). Fetuses were sacrificed at 80 days (n = 6) and 140 days (term, n = 10), comparing kidneys with normal controls of the same gestational age using immunohistochemical staining for β-catenin and CD10. Developing fetal cystic dysplastic kidneys were identified at 80 days. β-catenin staining showed the absence of granular cytoplasmic expression in cystic regions, indicating arrested nephrogenesis. In male models, cysts originated exclusively from proximal tubules. Female models exhibited mixed proximal and distal tubular involvement. CD10 staining confirmed the loss of proximal tubular markers. Renal development remained arrested at term. Cyst formation disrupts renal development early in gestation, which persists until term. Differences in cystogenesis between the models suggest that the site of obstruction influences pathogenic mechanisms. Full article
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