ArticleDiabetes2009
Specific local cardiovascular changes of Nepsilon-(carboxymethyl)lysine, vascular endothelial growth factor, and Smad2 in the developing embryos coincide with maternal diabetes-induced congenital heart defects.
Article in Diabetes, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 30 citations in OpenAlex.
- The roles of advanced glycation end products in cardiovascular diseases: from mechanisms to therapeutic strategies.Frontiers in cardiovascular medicine · 2025Review
- Embryonic Lethal Phenotyping to Identify Candidate Genes Related with Birth Defects.International journal of molecular sciences · 2024Article
- Early Methylglyoxal Exposure Leads to Worsened Cardiovascular Function in Young Rats.Nutrients · 2024Article
- Maternal Pre-Existing Diabetes: A Non-Inherited Risk Factor for Congenital Cardiopathies.International journal of molecular sciences · 2023Review
- Prevalence and risk factors for congenital heart defects among children in the Multi-Ethnic Yunnan Region of China.Translational pediatrics · 2022Article
- Outflow Tract Formation-Embryonic Origins of Conotruncal Congenital Heart Disease.Journal of cardiovascular development and disease · 2021Review
- Say NO to ROS: Their Roles in Embryonic Heart Development and Pathogenesis of Congenital Heart Defects in Maternal Diabetes.Antioxidants (Basel, Switzerland) · 2019Review
- microRNA expression profiling and functional annotation analysis of their targets modulated by oxidative stress during embryonic heart development in diabetic mice.Reproductive toxicology (Elmsford, N.Y.) · 2016Article
- Deregulated Cardiac Specific MicroRNAs in Postnatal Heart Growth.BioMed research international · 2016Article
- Superoxide Dismutase 1 In Vivo Ameliorates Maternal Diabetes Mellitus-Induced Apoptosis and Heart Defects Through Restoration of Impaired Wnt Signaling.Circulation. Cardiovascular genetics · 2015Article
- ASK1 mediates the teratogenicity of diabetes in the developing heart by inducing ER stress and inhibiting critical factors essential for cardiac development.American journal of physiology. Endocrinology and metabolism · 2015Article
- Importance of maternal diabetes on the chronological deregulation of the intrauterine development: an experimental study in rat.Journal of diabetes research · 2015Article
- TGFβ and Wnt in cardiac outflow tract defects in offspring of diabetic pregnancies.Birth defects research. Part B, Developmental and reproductive toxicology · 2014Article
- Disorders in glucidic metabolism and congenital heart diseases: detection and prevention.Pediatric cardiology · 2013Article
- Article
- Manifestation of renal disease in obesity: pathophysiology of obesity-related dysfunction of the kidney.International journal of nephrology and renovascular disease · 2009Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveEmbryos exposed to a diabetic environment in utero have an increased risk to develop congenital heart malformations. The mechanism behind the teratogenicity of diabetes still remains enigmatic. Detrimental effects of glycation products in diabetic patients have been well documented. We therefore studied a possible link between glycation products and the development of congenital cardiovascular malformations. Furthermore, we investigated other possible mechanisms involved in this pathogenesis: alterations in the levels of vascular endothelial growth factor (VEGF) or phosphorylated Smad2 (the latter can be induced by both glycation products and VEGF). RESEARCH DESIGN AND
methodsWe examined the temporal spatial patterning of the glycation products Nepsilon(carboxymethyl)lysine (CML) and methylglyoxal (MG) adducts, VEGF expression, and phosphorylated Smad2 during cardiovascular development in embryos from normal and diabetic rats.
resultsMaternal diabetes increased the CML accumulation in the areas susceptible to diabetes-induced congenital heart disease, including the outflow tract of the heart and the aortic arch. No MG adducts could be detected, suggesting that CML is more likely to be indicative for increased oxidative stress than for glycation. An increase of CML in the outflow tract of the heart was accompanied by an increase in phosphorylated Smad2, unrelated to VEGF. VEGF showed a time-specific decrease in the outflow tract of embryos from diabetic dams.
conclusionsFrom our results, we can conclude that maternal diabetes results in transient and localized alterations in CML, VEGF expression, and Smad2 phosphorylation overlapping with those regions of the developing heart that are most sensitive to diabetes-induced congenital heart disease.
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.