SynthesisScientific reports2015
Genetically-reduced serum ACE activity might be a causal risk factor for obstructive sleep apnea syndrome: A meta-analysis.
Synthesis in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.
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Who cites it
5 citing papers in PubMed, 1 synthesis or guideline pooled it, 13 citations in OpenAlex.
- Association of angiotensin-converting enzyme gene insertion/deletion polymorphism and obstructive sleep apnoea in a Chinese population: A meta-analysis.Journal of the renin-angiotensin-aldosterone system : JRAASPooled it
- The interaction among OSA, CPAP, and medications in patients with comorbid OSA and cardiovascular/cerebrovascular disease: a randomized controlled trial.BMC pulmonary medicine · 2022 · on this mapTrial
- Exploratory Associations of Targeted Genetic Variants with Cephalometric Airway Parameters in Children with Skeletal Class II Sleep-Disordered Breathing Symptoms.Children (Basel, Switzerland) · 2026Article
- Estimated prevalence of obstructive sleep apnea by occupation and industry in England: a descriptive study.Sleep advances : a journal of the Sleep Research Society · 2024Article
- Hypertension and longevity: role of genetic polymorphisms in renin-angiotensin-aldosterone system and endothelial nitric oxide synthase.Molecular and cellular biochemistry · 2019Observational
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We meta-analytically summarized the associations of angiotensin converting enzyme (ACE) gene insertion/deletion (I/D) polymorphism with ACE activity and obstructive sleep apnea syndrome (OSAS) to see whether ACE activity is causally associated with OSAS. Literature search and data abstraction were done in duplicate. Sixteen articles including 2060 OSAS patients and 1878 controls were summarized. Overall, no significance was observed for the association of I/D polymorphism with OSAS, whereas carriers of II genotype (weighted mean difference or WMD, 95% confidence interval or CI, P: -11.976, -17.168 to -6.783, <0.001) or I allele (-9.842, -14.766 to -4.918, <0.001) had a lower level of serum ACE activity compared with DD genotype carriers, respectively. In subgroup analyses, carriers of II genotype were 3.806 times more likely to develop OSAS (95% CI, P: 1.865 to 7.765, <0.001) in OSAS patients with hypertension, without heterogeneity. Mendelian randomization analysis indicated there was 37.4% (95% CI: 1.115 to 3.142) and 32.4% (1.106 to 2.845) increased risk of OSAS by a reduction of 1 U/L in ACE activity for the II genotype and I allele carriers versus DD genotype carriers, respectively. There was no observable publication bias. Collectively, genetically-reduced serum ACE activity might be a causal risk factor for OSAS.
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