ReviewNaunyn-Schmiedeberg's archives of pharmacology2026
Diabetic kidney disease: exploring mechanistic depths and the future of pharmacological intervention.
Review in Naunyn-Schmiedeberg's archives of pharmacology, 2026. 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.
- 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
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
Diabetic kidney disease (DKD) is the primary driver of chronic kidney disease (CKD) and end-stage renal disease (ESRD) globally and poses a major and escalating public health concern in the context of the diabetes epidemic. Despite current therapeutic interventions, a substantial residual risk of disease progression persists, emphasizing the necessity for improved treatment strategies. A comprehensive elucidation of the molecular mechanisms underlying DKD is crucial for developing novel therapies aimed at slowing disease progression and reducing associated complications. This review provides an in-depth overview of the evolution and present knowledge on DKD, established and emerging molecular mechanisms, and evolving therapeutic approaches. Recent advances have revealed a more complex pathophysiological landscape involving mitochondrial dysfunction and endoplasmic reticulum stress. By synthesizing recent developments in the field, this review highlights the significance of these interconnected mechanisms in DKD pathogenesis and proposes innovative, underexplored therapeutic options, including a novel SIRT1 activator, NLRP3 inhibitor, PLK2 inhibitor, ET1A antagonist, and curcumin derivative that hold potential in combating DKD. Ultimately, it underscores the critical need for continued research to address unresolved questions and to develop more effective, multitargeted interventions to improve outcomes for individuals with DKD.
Indexed as
Identifiers
40828323What 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.