ArticleJCI insight2018
Tyro3 is a podocyte protective factor in glomerular disease.
Article in JCI insight, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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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.
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Who cites it
18 citing papers in PubMed, 26 citations in OpenAlex.
- Semi-automated reconstruction of glomerular architecture from 3D confocal microscopy data.bioRxiv : the preprint server for biology · 2026Article
- Lysine-specific histone demethylase 1a regulates nephron development and long-term transcriptional programming.JCI insight · 2026Article
- Association of GAS6, AXL, and GAS6-AS lncRNAs with nephropathy in Egyptian patients with type 2 diabetes mellitus: a case-control observational study.Nutrition & diabetes · 2025Observational
- Pathway insights and predictive modeling for type 2 diabetes using polygenic risk scores.Scientific reports · 2025Article
- Adriamycin-induced nephropathy models: elucidating CKD pathophysiology and advancing therapeutic strategies.Experimental animals · 2025Review
- Identification of podocyte molecular markers in diabetic kidney disease via single-cell RNA sequencing and machine learning.PloS one · 2025Article
- Role and Mechanisms of Tyro3 in Podocyte Biology and Glomerular Disease.Kidney diseases (Basel, Switzerland) · 2024Review
- Cholesterol 25-Hydroxylase Protects Against Diabetic Kidney Disease by Regulating ADP Ribosylation Factor 4.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Flow-induced reprogramming of endothelial cells in atherosclerosis.Nature reviews. Cardiology · 2023Review
- Identifying causal serum protein-cardiometabolic trait relationships using whole genome sequencing.Human molecular genetics · 2023Article
- TYRO3 agonist as therapy for glomerular disease.JCI insight · 2023Article
- Network-based identification and prioritization of key transcriptional factors of diabetic kidney disease.Computational and structural biotechnology journal · 2023Article
- Signaling pathways of chronic kidney diseases, implications for therapeutics.Signal transduction and targeted therapy · 2022Review
- Sulfuretted hydrogen ameliorates high dose glucose-induced podocyte apoptosis via orchestrating AMPK/mTOR cascade-mediated anti-apoptotic effects.Annals of translational medicine · 2021Article
- P2Y2R contributes to the development of diabetic nephropathy by inhibiting autophagy response.Molecular metabolism · 2020Article
- Article
- Gas6/TAM Axis in Sepsis: Time to Consider Its Potential Role as a Therapeutic Target.Disease markers · 2019Review
- Post-Transplant Recurrence of Focal Segmental Glomerulosclerosis: Circulating Factors, Molecular Biomarkers, and Treatments.Kidney diseases (Basel, Switzerland)Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 7 institutions in 2 countries.
Funding
Abstract
Our previous work demonstrated a protective role of protein S in early diabetic kidney disease (DKD). Protein S exerts antiinflammatory and antiapoptotic effects through the activation of TYRO3, AXL, and MER (TAM) receptors. Among the 3 TAM receptors, we showed that the biological effects of protein S were mediated largely by TYRO3 in diabetic kidneys. Our data now show that TYRO3 mRNA expression is highly enriched in human glomeruli and that TYRO3 protein is expressed in podocytes. Interestingly, glomerular TYRO3 mRNA expression increased in mild DKD but was suppressed in progressive DKD, as well as in focal segmental glomerulosclerosis (FSGS). Functionally, morpholino-mediated knockdown of tyro3 altered glomerular filtration barrier development in zebrafish larvae, and genetic ablation of Tyro3 in murine models of DKD and Adriamycin-induced nephropathy (ADRN) worsened albuminuria and glomerular injury. Conversely, the induction of TYRO3 overexpression specifically in podocytes significantly attenuated albuminuria and kidney injury in mice with DKD, ADRN, and HIV-associated nephropathy (HIVAN). Mechanistically, TYRO3 expression was suppressed by activation of TNF-α/NF-κB pathway, which may contribute to decreased TYRO3 expression in progressive DKD and FSGS, and TYRO3 signaling conferred antiapoptotic effects through the activation of AKT in podocytes. In conclusion, TYRO3 plays a critical role in maintaining normal podocyte function and may be a potential new drug target to treat glomerular diseases.
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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.