ReviewNature reviews. Nephrology2024
Podocyte-targeted therapies - progress and future directions.
Review in Nature reviews. Nephrology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 2 of them syntheses that pooled it.
What it found
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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
52 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- Pooled it
- Evolutionary patterns and research frontiers in autophagy in podocytopathies: a bibliometric analysis.Frontiers in medicine · 2024Pooled it
- Clinical characteristics and prognosis of IgA nephropathy and comorbid diabetic kidney disease.Annals of medicine · 2026Article
- Nanotechnology-mediated podocyte injury repair: mechanistic exploration and therapeutic prospects.Renal failure · 2026Review
- The landscape of allele-specific expression in human kidneys.Science advances · 2026Article
- Cardiovascular-kidney-metabolic syndrome as a mitochondrial systems disorder.Nature reviews. Nephrology · 2026Review
- SPARC Drives Podocyte Mitochondrial Damage and Ferroptosis in Diabetic Kidney Disease Following Klotho Deficiency.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- WTAP Deficiency Promotes Podocyte PANoptosis and FSGS via SPP1 Signaling.Circulation research · 2026Article
- SnRNA-seq and genome-wide CRISPR screening define the complete transcriptional trajectory and functional drivers of podocyte stress.Cellular and molecular life sciences : CMLS · 2026Article
- New therapeutic hope for rare podocytopathies.Pediatric nephrology (Berlin, Germany) · 2026Article
- Exosomal miR-20a-5p derived from renal tubular epithelial cells regulates podocyte cytoskeletal remodeling via targeting myosin X in diabetic kidney disease.Diabetology & metabolic syndrome · 2026Article
- RENAL-CHIP: Rejection Evaluation via Non-Invasive Analysis of Circulating Podocytes With Herringbone-Chip Isolation Platform.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Mitochondrial Regulation of the NLRP3 Inflammasome in Diabetic Kidney Disease: From Mechanisms to Therapeutic Strategies.International journal of molecular sciences · 2026Review
- Interferon α-induced HERC6 provokes podocyte dysfunction via mitotic catastrophe in lupus nephritis.Arthritis research & therapy · 2026Article
- Obinutuzumab alone may be an effective option for adult minimal change disease: a single-center retrospective observational study.BMC nephrology · 2026Observational
- Podocyte TLR4 deletion alleviates diabetic kidney disease through prohibiting PKCδ/SHP-1-dependent ER stress and relieving podocyte damage and inflammation.Journal of advanced research · 2026Article
- Podocyte Metabolic Reprogramming and Targeted Therapy.Journal of the American Society of Nephrology : JASN · 2026Review
- SETDB2 Mitigates Podocyte Dysfunction in Diabetic Kidney Disease Through Epigenetic Silencing of SMAD3.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Gastrodin alleviates high fructose-induced podocyte mitochondria-mediated apoptosis by inhibiting NLRP6 to facilitate TRIM7-triggeredInternational journal of biological sciences · 2026Article
- Kidney-targeted drug delivery: from physiological mechanisms to precision therapeutics.Frontiers in bioengineering and biotechnology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Podocytes are the key target cells for injury across the spectrum of primary and secondary proteinuric kidney disorders, which account for up to 90% of cases of kidney failure worldwide. Seminal experimental and clinical studies have established a causative link between podocyte depletion and the magnitude of proteinuria in progressive glomerular disease. However, no substantial advances have been made in glomerular disease therapies, and the standard of care for podocytopathies relies on repurposed immunosuppressive drugs. The past two decades have seen a remarkable expansion in understanding of the mechanistic basis of podocyte injury, with prospects increasing for precision-based treatment approaches. Dozens of disease-causing genes with roles in the pathogenesis of clinical podocytopathies have been identified, as well as a number of putative glomerular permeability factors. These achievements, together with the identification of novel targets of podocyte injury, the development of potential approaches to harness the endogenous podocyte regenerative potential of progenitor cell populations, ongoing clinical trials of podocyte-specific pharmacological agents and the development of podocyte-directed drug delivery systems, contribute to an optimistic outlook for the future of glomerular disease therapy.
Indexed as
Identifiers
38724717What 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.