ReviewAmerican journal of translational research2025
The interplay between endothelial cell dysfunction and podocyte injury in diabetic nephropathy: a comprehensive review of current evidence.
Review in American journal of translational research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diabetic nephropathy (DN) remains the leading cause of end-stage renal disease globally. Emerging evidence highlights the bidirectional crosstalk between glomerular endothelial cell (GEC) dysfunction and podocyte injury as a key driver of DN progression. This review synthesizes current understanding of the molecular mechanisms, clinical correlations, and therapeutic strategies targeting this interplay. Mechanistically, hyperglycemia-induced oxidative stress, dysregulated angiogenesis, and aberrant extracellular vesicle (EV)-mediated signaling contribute to a self-perpetuating cycle of glomerular injury. Clinically, biomarkers of endothelial-podocyte axis disruption predict disease progression and therapeutic response. Novel therapies, including endothelin receptor antagonists, sodium-glucose cotransporter 2 (SGLT2) inhibitors, and mesenchymal stem cell derived EVs, show promise for restoring glomerular filtration barrier (GFB) integrity. This review integrates multi-omics insights to propose a unified model of DN pathogenesis and precision medicine approaches.
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Registered trials
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