ArticleCell death discovery2026
MAPK14/SLC7A11/GPX4 axis dysregulation drives podocyte ferroptosis via mediating glycerophospholipid metabolism.
Article in Cell death discovery, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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.
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Who cites it
4 citing papers in PubMed.
- Metformin protects podocytes by inhibiting the MAPK14-SLC7A11-GPX4 axis and dysregulation of fatty acid metabolism.Diabetologia · 2026Article
- Glycolytic lactylation modulates cell death decisions in diabetic kidney disease: Metabolic‑epigenetic interplay between ferroptosis and autophagy in fibrotic remodeling (Review).International journal of molecular medicine · 2026Review
- The dysregulated unfolded protein response in diabetic kidney disease: mechanisms and crosstalk with cell death pathways.Frontiers in pharmacology · 2026Review
- Integrated transcriptomic analysis of LMB2-induced podocyte injury identifies conserved inflammatory and adaptive stress responses.PloS one · 2026Article
Corrections and comments
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Authors and funding
17 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diabetic nephropathy (DN), the leading cause of end-stage renal disease, lacks effective therapies due to an incomplete understanding of its cell-type-specific pathogenesis. Here, through an integrative multi-omics approach, we have decoded the molecular architecture of DN, identify novel therapeutic targets, and validates a promising intervention. Single-cell RNA sequencing of human diabetic kidneys reveals the podocyte as the central cellular nexus of DN, exhibiting specific dysregulation in ferroptosis and glycerophospholipid metabolism, and possessing superior diagnostic potential. High-resolution analysis of podocyte heterogeneity identifies ferroptosis as a key driver of glomerular injury, centered on the dysregulated genes MAPK14/SLC7A11/GPX4. We further demonstrated that astragaloside IV (ASIV) exerts potential protective effects by specifically targeting the ferroptosis pathway, reversing the diabetic transcriptional landscape and preserving podocyte integrity. Spatial metabolomics uncovers profound anatomical compartmentalization of metabolic dysregulation in the renal cortex and medulla, which is effectively regulated by ASIV. Integrated transcriptomic and metabolomic profiling in vitro definitively establishes ferroptosis inhibition as the core mechanism of ASIV-mediated podocyte protection. Finally, clinical metabolomic profiling identifies urinary metabolic intermediates of glycerophospholipid metabolism as highly sensitive and specific non-invasive biomarkers for its diagnosis. Our study delineates a fundamental research framework for DN, from basic mechanism to targeted therapy and precision diagnostics.
Identifiers
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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 Socratic graph.