ReviewKidney international reports2025
Stanniocalcin-1: A Novel Mediator in Diabetic Kidney Disease and Cardiovascular Disease.
Review in Kidney international reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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
3 citing papers in PubMed.
- Article
- ElevatedCancer genomics & proteomics · 2025Article
- Advancing Understanding of Mitochondrial Function in Diabetic Kidney Disease.Kidney international reports · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diabetes mellitus represents a group of metabolic diseases characterized by hyperglycemia from defects in insulin secretion, action, or both. The prevalence of type 2 diabetes mellitus, characterized by insulin resistance, has increased over time in the UK, and is the most prevalent cause of chronic kidney disease (CKD). Cardiovascular complications are a major cause of mortality for these patients. Stanniocalcin (STC), originally identified in bony fish as a hormone regulating calcium levels, has since been found in mammals, including humans. In fish, STC functions as an antihypercalcemic factor. Mammals possess 2 STC orthologues, STC-1 and STC-2, with STC-1 demonstrating significant sequence and functional conservation across species. Unlike fish, STC-1 is not normally present in the blood of healthy humans. However, it can be detected in certain conditions such as pregnancy, cancer, and CKD. In humans, STC-1 has diverse roles, including modulation of calcium and phosphate homeostasis, and it is implicated in kidney and cardiovascular protection. It has been reported that STC-1 has antioxidant, anti-inflammatory, and antiapoptotic activities, playing a role in renoprotection in diabetic nephropathy. This review explores the molecular biology of STC-1, its physiological functions, and its emerging role in GKDs, particularly diabetic and cardiovascular diseases. We highlight its potential protective mechanisms against hypercalcemia, its antioxidant and anti-inflammatory properties, and its cardioprotective properties in ischemia-reperfusion. Further research into STC-1 could provide new insights into therapeutic strategies for managing diseases characterized by calcium imbalance and lead to new treatments for the cardiovascular morbidity associated with diabetic kidney disease.
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Registered trials
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