ArticleDevelopment (Cambridge, England)2021
Postnatal prolongation of mammalian nephrogenesis by excess fetal GDNF.
Article in Development (Cambridge, England), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
13 citing papers in PubMed, 17 citations in OpenAlex.
- Developmental origins of disease - Effects of iron deficiency in the rat developing kidney and beyond.Pediatric nephrology (Berlin, Germany) · 2026Review
- Fetal growth restriction leads to prolonged nephrogenesis and gene dysregulation in the adult kidney.Life science alliance · 2026Article
- Epigenetic regulation of kidney development.Nature reviews. Nephrology · 2026Review
- Preterm birth disrupts nephron progenitor cell dynamics predisposing to renal disease.iScience · 2026Article
- Early-Life Stress Programs a Vulnerable Renal Phenotype Under Metabolic Challenge in a Murine Model.Biomolecules · 2026Article
- Maternal nutrition can rapidly rescue a nephron deficit in low birthweight offspring.npj metabolic health and disease · 2025Article
- Nanobody Immunolabelling and three-dimensional imaging reveals spatially restricted LYVE1 expression by kidney lymphatic vessels in mice.Journal of nanobiotechnology · 2025Article
- Advances in pediatric acute kidney injury pathobiology: a report from the 26th Acute Disease Quality Initiative (ADQI) conference.Pediatric nephrology (Berlin, Germany) · 2024Article
- Article
- Regulation of nephron progenitor cell lifespan and nephron endowment.Nature reviews. Nephrology · 2022Review
- Omics profiling identifies the regulatory functions of the MAPK/ERK pathway in nephron progenitor metabolism.Development (Cambridge, England) · 2022Article
- Elevated endogenous GDNF induces altered dopamine signalling in mice and correlates with clinical severity in schizophrenia.Molecular psychiatry · 2022Article
- Protective role of endorepellin in renal developmental programming.Frontiers in cell and developmental biology · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nephron endowment, defined during the fetal period, dictates renal and related cardiovascular health throughout life. We show here that, despite its negative effects on kidney growth, genetic increase of GDNF prolongs the nephrogenic program beyond its normal cessation. Multi-stage mechanistic analysis revealed that excess GDNF maintains nephron progenitors and nephrogenesis through increased expression of its secreted targets and augmented WNT signaling, leading to a two-part effect on nephron progenitor maintenance. Abnormally high GDNF in embryonic kidneys upregulates its known targets but also Wnt9b and Axin2, with concomitant deceleration of nephron progenitor proliferation. Decline of GDNF levels in postnatal kidneys normalizes the ureteric bud and creates a permissive environment for continuation of the nephrogenic program, as demonstrated by morphologically and molecularly normal postnatal nephron progenitor self-renewal and differentiation. These results establish that excess GDNF has a bi-phasic effect on nephron progenitors in mice, which can faithfully respond to GDNF dosage manipulation during the fetal and postnatal period. Our results suggest that sensing the signaling activity level is an important mechanism through which GDNF and other molecules contribute to nephron progenitor lifespan specification.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.