| Literature DB >> 35036986 |
Xue Liu1, Ryan J Longchamps2, Kerri L Wiggins3, Laura M Raffield4, Lawrence F Bielak5, Wei Zhao5, Achilleas Pitsillides1, Thomas W Blackwell6, Jie Yao7, Xiuqing Guo7, Nuzulul Kurniansyah8, Bharat Thyagarajan9, Nathan Pankratz10, Stephen S Rich11, Kent D Taylor7, Patricia A Peyser5, Susan R Heckbert12, Sudha Seshadri13,14,15, L Adrienne Cupples1, Eric Boerwinkle16,17, Megan L Grove16, Nicholas B Larson18, Jennifer A Smith5, Ramachandran S Vasan14,19, Tamar Sofer8,20, Annette L Fitzpatrick21, Myriam Fornage22, Jun Ding23, Adolfo Correa24, Goncalo Abecasis6, Bruce M Psaty3,25, James G Wilson26, Daniel Levy14,27, Jerome I Rotter7, Joshua C Bis3, Claudia L Satizabal13,14,15, Dan E Arking2, Chunyu Liu1,14.
Abstract
Mitochondrial DNA (mtDNA) is present in multiple copies in human cells. We evaluated cross-sectional associations of whole blood mtDNA copy number (CN) with several cardiometabolic disease traits in 408,361 participants of multiple ancestries in TOPMed and UK Biobank. Age showed a threshold association with mtDNA CN: among younger participants (<65 years of age), each additional 10 years of age was associated with 0.03 standard deviation (s.d.) higher level of mtDNA CN (P = 0.0014) versus a 0.14 s.d. lower level of mtDNA CN (P = 1.82 × 10-13) among older participants (≥65 years). At lower mtDNA CN levels, we found age-independent associations with increased odds of obesity (P = 5.6 × 10-238), hypertension (P = 2.8 × 10-50), diabetes (P = 3.6 × 10-7), and hyperlipidemia (P = 6.3 × 10-5). The observed decline in mtDNA CN after 65 years of age may be a key to understanding age-related diseases.Entities:
Year: 2021 PMID： 35036986 PMCID： PMC8758111 DOI： 10.1016/j.xgen.2021.100006
Source DB: PubMed Journal: Cell Genom ISSN： 2666-979X