ArticleBlood advances2021
Search for AL amyloidosis risk factors using Mendelian randomization.
Article in Blood advances, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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.
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Who cites it
5 citing papers in PubMed, 11 citations in OpenAlex.
- The molecular landscape of AL amyloidosis.British journal of haematology · 2025Review
- Exploring the role of circulating proteins in multiple myeloma risk: a Mendelian randomization study.Scientific reports · 2025Article
- Subtyping based on immune cell fractions reveal heterogeneity of cardiac fibrosis in end-stage heart failure.Frontiers in immunology · 2023Article
- U-Shaped Association Between Monocyte-Lymphocyte Ratio and Risk of Cardiac Conduction Block.Journal of inflammation research · 2023Article
- T cell landscape and dynamics in immunoglobulin light chain amyloidosis before and after daratumumab-based therapy.Clinical and translational medicine · 2021Article
Corrections and comments
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Authors and funding
21 authors at 9 institutions in 6 countries.
Funding
Abstract
In amyloid light chain (AL) amyloidosis, amyloid fibrils derived from immunoglobulin light chain are deposited in many organs, interfering with their function. The etiology of AL amyloidosis is poorly understood. Summary data from genome-wide association studies (GWASs) of multiple phenotypes can be exploited by Mendelian randomization (MR) methodology to search for factors influencing AL amyloidosis risk. We performed a 2-sample MR analyzing 72 phenotypes, proxied by 3461 genetic variants, and summary genetic data from a GWAS of 1129 AL amyloidosis cases and 7589 controls. Associations with a Bonferroni-defined significance level were observed for genetically predicted increased monocyte counts (P = 3.8 × 10-4) and the tumor necrosis factor receptor superfamily member 17 (TNFRSF17) gene (P = 3.4 × 10-5). Two other associations with the TNFRSF (members 6 and 19L) reached a nominal significance level. The association between genetically predicted decreased fibrinogen levels may be related to roles of fibrinogen other than blood clotting. be related to its nonhemostatic role. It is plausible that a causal relationship with monocyte concentration could be explained by selection of a light chain-producing clone during progression of monoclonal gammopathy of unknown significance toward AL amyloidosis. Because TNFRSF proteins have key functions in lymphocyte biology, it is entirely plausible that they offer a potential link to AL amyloidosis pathophysiology. Our study provides insight into AL amyloidosis etiology, suggesting high circulating levels of monocytes and TNFRSF proteins as risk factors.
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