ArticleAging cell2017
Transthyretin deposition promotes progression of osteoarthritis.
Article in Aging cell, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
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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
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.
- Meta-analysis Integrated With Multi-omics Data Analysis to Elucidate Pathogenic Mechanisms of Age-Related Knee Osteoarthritis in Mice.The journals of gerontology. Series A, Biological sciences and medical sciences · 2022Pooled it
- HCCaging: a liver physiological aging-related biomarker for hepatocellular carcinoma diagnosis based on transcriptome data.npj aging · 2026Article
- Changes in the concentration of phosphatidylcholine in lipid bilayers determines the aggregation rate of transthyretin.Biophysical chemistry · 2026Article
- Plasma Proteomics Reveals Persistent and Surgery-Responsive Molecular Signatures in Osteoarthritis Patients.International journal of molecular sciences · 2026Article
- Associations between pathophysiological traits and symptom development in retrospective analysis of V30M and V122I transthyretin amyloidosis.International journal of cardiology. Heart & vasculature · 2025Article
- Differential Expression of Fibrinogen Alpha and Its Potential Involvement in Osteoarthritis Pathogenesis.Molecular biotechnology · 2025Article
- Plasmalogens Alter the Aggregation Rate of Transthyretin and Lower Toxicity of Transthyretin Fibrils.The journal of physical chemistry letters · 2024Article
- Cholesterol and Sphingomyelin Uniquely Alter the Rate of Transthyretin Aggregation and Decrease the Toxicity of Amyloid Fibrils.The journal of physical chemistry letters · 2023Article
- Nanoscale structural characterization of transthyretin aggregates formed at different time points of protein aggregation using atomic force microscopy-infrared spectroscopy.Protein science : a publication of the Protein Society · 2023Article
- Saturation of fatty acids in phosphatidic acid uniquely alters transthyretin stability changing morphology and toxicity of amyloid fibrils.Chemistry and physics of lipids · 2023Article
- The clusterin connectome: Emerging players in chondrocyte biology and putative exploratory biomarkers of osteoarthritis.Frontiers in immunology · 2023Article
- Resolution therapy: Harnessing efferocytic macrophages to trigger the resolution of inflammation.Frontiers in immunology · 2022Review
- Review
- Transthyretin amyloid deposits in lumbar spinal stenosis and assessment of signs of systemic amyloidosis.Journal of internal medicine · 2021Article
- Article
- Catalytic antibody (catabody) platform for age-associated amyloid disease: From Heisenberg's uncertainty principle to the verge of medical interventions.Mechanisms of ageing and development · 2020Review
- Wild-type transthyretin cardiac amyloidosis: a case of multisystemic involvement and review of literature.Romanian journal of morphology and embryology = Revue roumaine de morphologie et embryologieReview
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Deposition of amyloid is a common aging-associated phenomenon in several aging-related diseases. Osteoarthritis (OA) is the most prevalent joint disease, and aging is its major risk factor. Transthyretin (TTR) is an amyloidogenic protein that is deposited in aging and OA-affected human cartilage and promotes inflammatory and catabolic responses in cultured chondrocytes. Here, we investigated the role of TTR in vivo using transgenic mice overexpressing wild-type human TTR (hTTR-TG). Although TTR protein was detected in cartilage in hTTR-TG mice, the TTR transgene was highly overexpressed in liver, but not in chondrocytes. OA was surgically induced by destabilizing the medial meniscus (DMM) in hTTR-TG mice, wild-type mice of the same strain (WT), and mice lacking endogenous Ttr genes. In the DMM model, both cartilage and synovitis histological scores were significantly increased in hTTR-TG mice. Further, spontaneous degradation and OA-like changes in cartilage and synovium developed in 18-month-old hTTR mice. Expression of cartilage catabolic (Adamts4, Mmp13) and inflammatory genes (Nos2, Il6) was significantly elevated in cartilage from 6-month-old hTTR-TG mice compared with WT mice as was the level of phospho-NF-κB p65. Intra-articular injection of aggregated TTR in WT mice increased synovitis and significantly increased expression of inflammatory genes in synovium. These findings are the first to show that TTR deposition increases disease severity in the murine DMM and aging model of OA.
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Registered trials
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