ArticleACS pharmacology & translational science2026
Nesfatin‑1 Deficiency Exacerbates Calcium Oxalate Monohydrate-Induced Cellular Injury in Renal Epithelial Cells.
Article in ACS pharmacology & translational science, 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
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Calcium oxalate monohydrate (COM) crystals are major contributors to nephrolithiasis-associated renal tubular injury, primarily through mechanisms involving oxidative stress, inflammation, apoptosis, and epithelial-mesenchymal transition (EMT). While nesfatin-1 is known for its antioxidant and cytoprotective actions, the specific role of endogenous nesfatin-1 in regulating COM-induced epithelial injury has not been fully defined. In this study, nesfatin-1 was silenced using antisense oligonucleotides in NRK-52E and primary renal tubular epithelial cells to examine how loss of endogenous nesfatin-1 peptide influences cellular susceptibility to COM. COM exposure reduced nesfatin-1 levels, and this decline was markedly greater in the nesfatin-1 silenced + COM group. Silencing nesfatin-1 intensified COM-driven oxidative stress, as reflected by reduced catalase activity and increased levels of malondialdehyde, nitric oxide, and ROS. Pro-inflammatory markers including NF-κB, TNF-α, IL-6, and IL-1β were upregulated, whereas IL-10 was decreased. Apoptotic indicators such as elevated intracellular Ca
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.