ArticleScientific reports2017
Inflammatory state exists in familial amyloid polyneuropathy that may be triggered by mutated transthyretin.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 18 citations in OpenAlex.
- Associations between pathophysiological traits and symptom development in retrospective analysis of V30M and V122I transthyretin amyloidosis.International journal of cardiology. Heart & vasculature · 2025Article
- Characterization of Transthyretin Mutation G47V Associated with Hereditary Cardiac Amyloidosis.Cardiology · 2024Article
- Review
- Inflammation across the spectrum of hypertrophic cardiac phenotypes.Heart failure reviews · 2023Review
- Microcalcification andInternational journal of molecular sciences · 2023Article
- Serum Inflammatory Profile in Hereditary Transthyretin Amyloidosis: Mechanisms and Possible Therapeutic Implications.Brain sciences · 2022Article
- ATTR amyloidosis during the COVID-19 pandemic: insights from a global medical roundtable.Orphanet journal of rare diseases · 2021Article
- Plasma growth differentiation factor 15: a novel tool to detect early changes of hereditary transthyretin amyloidosis.ESC heart failure · 2021Article
- Impaired in vitro growth response of plasma-treated cardiomyocytes predicts poor outcome in patients with transthyretin amyloidosis.Clinical research in cardiology : official journal of the German Cardiac Society · 2021Article
- Elevated interleukin-6 levels are associated with impaired outcome in cardiac transthyretin amyloidosis.World journal of cardiology · 2021Article
- Etiological Value of Sterile Inflammation in Preeclampsia: Is It a Non-Infectious Pregnancy Complication?Frontiers in cellular and infection microbiology · 2021Review
- A cell-based high-throughput screening method to directly examine transthyretin amyloid fibril formation at neutral pH.The Journal of biological chemistry · 2019Article
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The relationship between familial amyloid polyneuropathy (FAP), which is caused by mutated transthyretin (TTR), and inflammation has only recently been noted. To determine whether inflammation is present in FAP carriers and patients, serum interleukin (IL)-6 concentration in 57 healthy donors (HD), 21 FAP carriers, and 66 FAP patients was examined, with the relationship between IL-6 and TTR assessed in each group by multiple regression analysis and structural equation models (SEM). Compared with HD, IL-6 concentration was elevated in FAP carriers (p = 0.001, 95% CI 0.398-1.571) and patients (p = 0.002, 95% CI 0.362-1.521). Further, SEM indicated a positive relationship between IL-6 and TTR in FAP carriers (p = 0.010, 95% CI 0.019-0.140), but not in HD and FAP patients. In addition, we determined whether TTR induces production of pro-inflammatory cytokines ex vivo. HD-derived CD14 + monocytes and induced pluripotent stem cell-derived myeloid lineage cells from a HD and FAP patient dose-dependently produced IL-6 under mutated and aggregated TTR conditions, compared with wild-type TTR. In conclusion, FAP carriers and patients are in an inflammatory state, with the presence of mutated TTR being a trigger of inflammation, especially in FAP carriers.
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