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Adiponectin-mediated regulation of the adiponectin cascade in cardiovascular disease: Updates.
Hafiane, Anouar.
Afiliação
  • Hafiane A; Research Institute, McGill University Health Center, Montreal, QC, Canada. Electronic address: anouar.hafiane@mail.mcgill.ca.
Biochem Biophys Res Commun ; 694: 149406, 2024 Jan 29.
Article em En | MEDLINE | ID: mdl-38134479
ABSTRACT
The endocrine function of white adipose tissue is characterized by the synthesis of one its main hormones adiponectin. Although the biological role of adiponectin has not been fully defined, clinical and experimental observations have shown that low plasma concentrations of adiponectin participate in the prevalence of insulin resistance and cardiovascular diseases, mainly in obese patients. Adiponectin also exerts its effects on the heart and blood vessels, thereby influencing their physiology. Studying the effects of adiponectin presents some complexities, primarily due to potential cross-interactions and interference with other pathways, such as the AdipoR1/R2 pathways. Under optimal conditions, the activation of the adiponectin cascade may involve signals such as AMPK and PPARα. Interestingly, these pathways may trigger similar responses, such as fatty acid oxidation. Understanding the downstream effectors of these pathways is crucial to comprehend the extent to which adiponectin signaling impacts metabolism. In this review, the aim is to explore the current mechanisms that regulate the adiponectin pathways. Additionally, updates on the major downstream factors involved in adiponectin signaling are provided, specifically in relation to metabolic syndrome and atherosclerosis.
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Texto completo: 1 Base de dados: MEDLINE Assunto principal: Resistência à Insulina / Doenças Cardiovasculares / Síndrome Metabólica Limite: Humans Idioma: En Ano de publicação: 2024 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Resistência à Insulina / Doenças Cardiovasculares / Síndrome Metabólica Limite: Humans Idioma: En Ano de publicação: 2024 Tipo de documento: Article