{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,6]],"date-time":"2026-03-06T19:38:07Z","timestamp":1772825887717,"version":"3.50.1"},"reference-count":76,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"3","funder":[{"DOI":"10.13039\/100017954","name":"Fujian Provincial Finance Department","doi-asserted-by":"crossref","award":["BPB-2023SJZ"],"award-info":[{"award-number":["BPB-2023SJZ"]}],"id":[{"id":"10.13039\/100017954","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":[],"abstract":"<jats:title>Abstract:<\/jats:title>\n          <jats:p>Transthyretin amyloidosis (ATTR) is characterized by the deposition of unstable transthyretin protein (TTR) in the heart or peripheral nerves. Therapeutic strategies for ATTR include inhibition of the secretion of abnormal TTR by the liver, reducing the concentration of aberrant TTR in the circulation, and eliminating amyloid deposits of TTR in tissues. This article delves into the pathogenesis of TTR secretion from the liver into the bloodstream, its deposition in tissues, and the subsequent development of ATTR. In addition, we delineated the advancements in treatment strategies and discussed future research directions to provide novel insights for the identification of diagnostic and preventive targets.<\/jats:p>","DOI":"10.1097\/fjc.0000000000001663","type":"journal-article","created":{"date-parts":[[2024,12,31]],"date-time":"2024-12-31T17:00:35Z","timestamp":1735664435000},"page":"186-193","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":1,"title":["Advances in Studying the Pathologic Mechanisms and Treatment Strategies of Transthyretin Amyloidosis"],"prefix":"10.1097","volume":"85","author":[{"ORCID":"https:\/\/orcid.org\/0009-0009-8979-951X","authenticated-orcid":false,"given":"Hongyin","family":"Chen","sequence":"first","affiliation":[{"name":"Fujian Medical University, Fuzhou, China;"},{"name":"Department of Cardiology, The First Affiliated Hospital of Fujian Medical University, Fuzhou, China;"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ruonan","family":"Liu","sequence":"additional","affiliation":[{"name":"Fujian Medical University, Fuzhou, China;"},{"name":"Department of Cardiology, The First Affiliated Hospital of Fujian Medical University, Fuzhou, China;"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Siqi","family":"Luo","sequence":"additional","affiliation":[{"name":"Department of Rehabilitation Medicine, The First Affiliated Hospital of Fujian Medical University, Fuzhou, China; and"},{"name":"Department of Rehabilitation Medicine, National Regional Medical Center, Bihai Campus of the First Affiliated Hospital, Fujian Medical University, Fuzhou, China."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jinzi","family":"Su","sequence":"additional","affiliation":[{"name":"Department of Cardiology, The First Affiliated Hospital of Fujian Medical University, Fuzhou, China;"},{"name":"Department of Rehabilitation Medicine, National Regional Medical Center, Bihai Campus of the First Affiliated Hospital, Fujian Medical University, Fuzhou, China."}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"276","published-online":{"date-parts":[[2025,3]]},"reference":[{"key":"R1-20250306","doi-asserted-by":"crossref","first-page":"25","DOI":"10.3390\/ijms23010025","article-title":"Molecular mechanisms of cardiac amyloidosis","volume":"23","author":"Saito","year":"2021","journal-title":"Int J Mol Sci"},{"key":"R2-20250306","doi-asserted-by":"crossref","first-page":"1242815","DOI":"10.3389\/fneur.2023.1242815","article-title":"Hereditary transthyretin amyloidosis: a comprehensive review with a focus on peripheral neuropathy","volume":"5","author":"Poli","year":"2023","journal-title":"Front Neurol"},{"key":"R3-20250306","doi-asserted-by":"crossref","first-page":"1610","DOI":"10.1253\/circj.CJ-20-0110","article-title":"JCS 2020 guideline on diagnosis and treatment of cardiac amyloidosis","volume":"84","author":"Kitaoka","year":"2020","journal-title":"Circ J"},{"key":"R4-20250306","doi-asserted-by":"crossref","first-page":"17","DOI":"10.1016\/j.lpm.2009.02.021","article-title":"Liver transplantation for familial amyloid polyneuropathy","volume":"39","author":"Adams","year":"2010","journal-title":"La Presse M\u00e9dicale"},{"key":"R5-20250306","doi-asserted-by":"crossref","first-page":"11","DOI":"10.1056\/NEJMoa1716153","article-title":"Patisiran, an RNAi therapeutic, for hereditary transthyretin amyloidosis","volume":"379","author":"Adams","year":"2018","journal-title":"N Engl J Med"},{"key":"R6-20250306","doi-asserted-by":"crossref","first-page":"469","DOI":"10.1016\/j.jmb.2005.11.051","article-title":"Retention of misfolded mutant transthyretin by the chaperone BiP\/GRP78 mitigates amyloidogenesis","volume":"356","author":"S\u00f6rgjerd","year":"2006","journal-title":"J Mol Biol"},{"key":"R7-20250306","doi-asserted-by":"crossref","first-page":"8312","DOI":"10.1074\/jbc.M809354200","article-title":"The endoplasmic reticulum-associated degradation of transthyretin variants is negatively regulated by BiP in mammalian cells","volume":"284","author":"Susuki","year":"2009","journal-title":"J Biol Chem"},{"key":"R8-20250306","doi-asserted-by":"crossref","first-page":"1421","DOI":"10.1007\/s00018-019-03357-1","article-title":"Cellular secretion and cytotoxicity of transthyretin mutant proteins underlie late-onset amyloidosis and neurodegeneration","volume":"77","author":"Ibrahim","year":"2020","journal-title":"Cell Mol Life Sci"},{"key":"R9-20250306","doi-asserted-by":"crossref","first-page":"2283","DOI":"10.1096\/fj.11-189571","article-title":"Why are some amyloidoses systemic? 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