ArticleFrontiers in immunology2022
Association between genetically predicted leukocyte telomere length and non-scarring alopecia: A two-sample Mendelian randomization study.
Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 14 citations in OpenAlex.
- Decoding the gut microbiota-mitochondrial-inflammasome axis in cardiovascular disease.Molecular and cellular biochemistry · 2026Review
- Precision therapeutics in non-scarring alopecia: a systemic genomic and pathway-based framework for targeted interventions.ADMET & DMPK · 2026Review
- Exploring the causal relationship between iron status and subarachnoid hemorrhage based on two sample mendelian randomization.Scientific reports · 2025Article
- Loss of Ten1 in mice induces telomere shortening and models human dyskeratosis congenita.Science advances · 2025Article
- Telomere Length as Both Cause and Consequence in Type 1 Diabetes: Evidence from Bidirectional Mendelian Randomization.Biomedicines · 2025Article
- Stenotrophomonas maltophilia: An Urgent Threat with Increasing Antibiotic Resistance.Current microbiology · 2023Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
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Abstract
Background: The most commonly acknowledged non-scarring alopecia are androgenetic alopecia (AGA) and alopecia areata (AA). Previous studies have revealed various risk factors associated with alopecia. However, the relationship between leukocyte telomere length (LTL) and non-scarring alopecia remains unclear. Methods: A two-sample Mendelian randomization (MR) analysis was performed to evaluate the causality between genetically predicted LTL and the risk of non-scarring alopecia. MR analyses were performed using the inverse variance-weighted (IVW) method and complemented with other MR methods. Results: The summary statistics of the genome-wide association studies (GWAS) for AGA and AA were obtained from the FinnGen biobank, which included 119,185 and 211,428 individuals, respectively. A total of 126 single nucleotide polymorphisms (SNPs) with genome-wide significance were selected as the instrumental variables for LTL. The MR analyses suggested a causal relationship between LTL and AGA, and the risk of AGA increased by 3.19 times as the genetically predicted LTL was shortened by one standard deviation in log transformed form under the IVW method (OR = 4.19, 95% CI = 1.20-14.61, Conclusion: Our results suggested a potential causal relationship between LTL and AGA, and shortened LTL was associated with an increased risk of AGA.
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