Objective: This study aimed to systematically evaluate the effect of an angiotensin-converting enzyme (ACE) insertion/deletion (I/D) gene polymorphism on type 1 diabetic nephropathy (DN).
Methods: Cochrane Library, Embase, PubMed, Science Direct, Web of science, Wanfang data, VIP database, China Knowledge Resource Integrated Database, and SinoMed were searched. A total of 17 case-control studies analyzing ACE I/D polymorphism and type 1 DN risk were included in the present meta-analysis.
Results: Overall, a significant increased risk was found in allele comparison (OR = 1.16, 95% CI = 1.05-1.28, p = 0.04), dominant comparison (OR = 1.56, 95% CI = 1.14-2.15, p = 0.006) and homozygote comparison (OR = 1.52, 95% CI = 1.06-2.19, p = 0.02). In subgroup analyses according to ethnicity, the risk of type 1 DN in Asian population was increased in allele comparison (OR = 1.98, 95% CI = 1.15-3.42, p = 0.01), recessive comparison (OR = 2.48, 95% CI = 1.51-4.10, p = 0.0004), dominant comparison (OR = 3.15, 95% CI = 1.90-5.23, p < 0.00001), and homozygote comparison (OR = 2.87, 95% CI = 1.02-8.06, p = 0.05). However, there was no association between the ACE I/D genetic variants and type 1 DN in Caucasian populations.
Conclusions: Our meta-analysis results indicate that the ACE I/D polymorphism may contribute to type 1 DN development, especially in the Asian groups with type 1 diabetes. The current findings need to be confirmed by future well-designed and larger sample size primary studies in populations with different ethnicities.
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http://dx.doi.org/10.1080/0886022X.2016.1216707 | DOI Listing |
Acta Physiol (Oxf)
February 2025
Department of Biochemistry, Cell and Systems Biology, Institute of Systems, Molecular and Integrative Biology, Faculty of Health and Life Sciences, University of Liverpool, Liverpool, UK.
Aim: Long QT syndrome (LQTS) and catecholaminergic polymorphism ventricular tachycardia (CPVT) are inherited cardiac disorders often caused by mutations in ion channels. These arrhythmia syndromes have recently been associated with calmodulin (CaM) variants. Here, we investigate the impact of the arrhythmogenic variants D131E and Q135P on CaM's structure-function relationship.
View Article and Find Full Text PDFEur J Med Res
January 2025
Department of Anesthesiology, Chongqing Health Center for Women and Children, Women and Children's Hospital of Chongqing Medical University, No. 120, Longshan Road, Yubei District, Chongqing, 401147, China.
Background: Postoperative pain intensity is influenced by various factors, including genetic variations. The SCN10A gene encodes the Nav1.8 sodium channel protein, which is crucial for pain signal transmission in peripheral sensory neurons.
View Article and Find Full Text PDFSci Rep
January 2025
Sexually Transmitted and Bloodborne Infections Surveillance and Molecular Epidemiology, Sexually Transmitted and Bloodborne Infections Division at the JC Wilt Infectious Diseases Research Centre, National Microbiology Laboratories, Public Health Agency of Canada, Winnipeg, MB, R3E 3L5, Canada.
Human Immunodeficiency Virus Type 1 (HIV) set-point viral load is a strong predictor of disease progression and transmission risk. A recent genome-wide association study in individuals of African ancestries identified a region on chromosome 1 significantly associated with decreased HIV set-point viral load. Knockout of the closest gene, CHD1L, enhanced HIV replication in vitro in myeloid cells.
View Article and Find Full Text PDFTransl Psychiatry
January 2025
Research Center Juelich, Institute of Neuroscience and Medicine 10, Research Center Juelich, Juelich, Germany.
Genetic variation in the α5 nicotinic acetylcholine receptor (nAChR) subunit of mice results in behavioral deficits linked to the prefrontal cortex (PFC). rs16969968 is the primary Single Nucleotide Polymorphism (SNP) in CHRNA5 strongly associated with nicotine dependence and schizophrenia in humans. We performed single cell-electrophysiology combined with morphological reconstructions on layer 6 (L6) excitatory neurons in the medial PFC (mPFC) of wild type (WT) rats, rats carrying the human coding polymorphism rs16969968 in Chrna5 and α5 knockout (KO) rats.
View Article and Find Full Text PDFEnviron Pollut
January 2025
Center for Endemic Disease Control, Chinese Center for Disease Control and Prevention, Harbin Medical University, Harbin, People's Republic of China; NHC Key Laboratory of Etiology and Epidemiology(Harbin Medical University); Joint Key Laboratory of Endemic Diseases(Harbin Medical University, Guizhou Medical University, Xi'an Jiaotong University); Center for Chronic Disease Prevention and Control, Harbin Medical University, Harbin, People's Republic of China. Electronic address:
Background: Skeletal fluorosis is a chronic metabolic bone disease caused by excessive accumulation of fluoride in the bones. Previous studies have found that when the intake of tea fluoride is similar, the prevalence of skeletal fluorosis varies greatly among different ethnic groups, which may be related to different genetic backgrounds. Single nucleotide polymorphisms (SNPs) of estrogen receptor 1 (ESR1) and collagen type 1 α1 (COL1A1) were strongly associated with bone metabolism as well as bone growth and development, but their association with the risk of skeletal fluorosis has not been reported.
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