ReviewJournal of cardiovascular translational research2012
Does familial clustering of risk factors for long-term diabetic complications leave any place for genes that act independently?
Review in Journal of cardiovascular translational research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed, 8 citations in OpenAlex.
- Diabetic Microvascular Disease: An Endocrine Society Scientific Statement.The Journal of clinical endocrinology and metabolism · 2017Review
- Lymphoblastoid Cell Lines as a Tool to Study Inter-Individual Differences in the Response to Glucose.PloS one · 2016Article
- Genetics in diabetic retinopathy: current concepts and new insights.Current genomics · 2013Article
- Diabetic complications: current challenges and opportunities.Journal of cardiovascular translational research · 2012Article
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 at 2 institutions in 1 country.
Funding
Abstract
Long-term complications of type 1 diabetes, including nephropathy and retinopathy, share diabetes duration and hyperglycemia as major risk factors. Cross-sectional studies of sibpairs, both with type 1 diabetes, have shown familial clustering of specific complications, leading to the hypothesis that there are genetic contributors. However, because of the cross-sectional design of these studies, they were not able to account for the long-term effect of glycemia. Glycemia, measured by HbA1c, is correlated in sibs with type 1 diabetes. Recently, specific genetic loci that are associated with differences in HbA1c between people with type 1 diabetes have been convincingly identified, and they have also been shown to be associated with diabetic complications. This raises the question: how much of the familial clustering of diabetic complications is due to genes that influence risk without acting through the conventional risk factors? Implications for the design of genetic studies of diabetic complications are discussed.
Indexed as
Identifiers
What 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.