ArticleFrontiers in pharmacology2026
Targeting DPP9 attenuates podocyte injury by regulating NRF2 antioxidant signaling.
Article in Frontiers in pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Podocyte injury is a critical event in the progression of chronic kidney disease (CKD), with oxidative stress as a central pathogenic mechanism. Despite the efficacy of finerenone in mitigating CKD progression, its precise cytoprotective mechanisms within podocytes remain incompletely defined. This study aimed to elucidate the role of dipeptidyl peptidase 9 (DPP9) in podocyte injury and determine whether finerenone exerts its renoprotective effects via DPP9-mediated antioxidant effects. Methods: Integrated bioinformatic analyses of single-cell and bulk transcriptomic databases (KIT, NephroSeq) were performed, with validation in renal biopsies from patients with diabetic kidney disease (DKD) and in murine models of DKD and adriamycin-induced nephropathy. Results: DPP9 was significantly downregulated in injured podocytes from both human and murine models. DPP9 overexpression activated NRF2-mediated antioxidant responses, protecting podocytes from injury, whereas DPP9 depletion exacerbated cellular damage. Finerenone upregulated DPP9 protein levels, which subsequently enhanced DPP9-KEAP1 binding and competitively disrupted the NRF2-KEAP1 interaction, leading to NRF2 stabilization and activation. Consequently, finerenone improved renal function and alleviated pathological damage Conclusion: This study identifies DPP9 as a critical mediator of podocyte antioxidant defense and establishes that the therapeutic efficacy of finerenone is, at least in part, dependent on the upregulation of DPP9.
Indexed as
Identifiers
What Socratic 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 Socratic graph.