Hyperlipidemia and hypothyroidism.
Angiopoietin-like protein
Fibroblast growth factor
Hyperlipidemia
Hypothyroidism
PCSK9
Journal
Clinica chimica acta; international journal of clinical chemistry
ISSN: 1873-3492
Titre abrégé: Clin Chim Acta
Pays: Netherlands
ID NLM: 1302422
Informations de publication
Date de publication:
15 Feb 2022
15 Feb 2022
Historique:
received:
29
09
2021
revised:
09
01
2022
accepted:
10
01
2022
pubmed:
18
1
2022
medline:
15
2
2022
entrez:
17
1
2022
Statut:
ppublish
Résumé
Hypothyroidism is closely associated with increased serum total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C) and triglyceride (TG). The thyroid gland plays an important role in this process because thyroid hormones (THs) modulate cholesterol production, transformation and clearance. Although recent evidence suggests that thyroid-stimulating hormone (TSH) itself also participates in hyperlipidemia, the underlying mechanism remains unclear. Others demonstrated that the pathologic development of hypothyroidism-related hyperlipidemia was associated with down-regulated THs and up-regulated TSH in serum. This finding suggests a role for hypothyroidism in hyperlipidemia and potentially in related cardio-metabolic disease. Multiple newly identified modulatory biomarkers, such as proprotein convertase subtilisin/kexin type 9 (PCSK9), angiopoietin-like protein (ANGPTLs), and fibroblast growth factors (FGFs), might play a role in modulating the risk of hyperlipidemia induced by hypothyroidism. Moreover, hypothyroidism also contributes to the production of dysfunctional high-density lipoprotein (HDL) particles. In the present review, we examine the relationship between hypothyroidism with the risk and pathologic development of hyperlipidemia. We explore mechanisms by which hypothyroidism promotes hyperlipidemia in general and its contribution to cardio-metabolic disease specifically.
Identifiants
pubmed: 35038435
pii: S0009-8981(22)00015-8
doi: 10.1016/j.cca.2022.01.006
pii:
doi:
Substances chimiques
Cholesterol, LDL
0
PCSK9 protein, human
EC 3.4.21.-
Proprotein Convertase 9
EC 3.4.21.-
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
61-70Informations de copyright
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