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Omentin-1 As a Promising Biomarker and Therapeutic Target in Hypertension and Heart Failure: A Comprehensive Review Publisher



Zamanian MY1, 2 ; Maleki S3, 4 ; Oghenemaro EF5 ; Singh M6 ; Mohammadi M7 ; Alkhayyat AH8, 9, 10 ; Sapaev IB11, 12, 13 ; Kaur P14 ; Shirsalimi N2 ; Nagarwal A15
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Source: Naunyn-Schmiedeberg's Archives of Pharmacology Published:2025


Abstract

Omentin-1, a novel adipocytokine predominantly secreted by visceral adipose tissue, has emerged as a significant factor in cardiovascular health, particularly regarding hypertension (HTN) and heart failure (HF). This manuscript investigates the multifaceted roles of omentin-1 in these conditions, emphasizing its protective effects on vascular function and its potential as both a biomarker and therapeutic target. Clinical studies indicate that reduced circulating levels of omentin-1 are associated with metabolic syndrome (MetS) and increased cardiovascular risk, while animal studies demonstrate its ability to ameliorate endothelial dysfunction and lower blood pressure. Omentin-1 exerts its beneficial effects through various signaling pathways, including AMP-activated protein kinase (AMPK) and protein kinase B (Akt), thereby promoting vasodilation, enhancing insulin sensitivity, and mitigating inflammation. In the context of HF, particularly heart failure with preserved ejection fraction (HFpEF), omentin-1 levels exhibit a negative correlation with diastolic dysfunction and inflammatory markers, suggesting its role in cardiac protection. Additionally, the manuscript discusses the implications of omentin-1 in managing obesity-related cardiovascular diseases and its potential utility as a prognostic marker for adverse outcomes in HF patients. Collectively, omentin-1 represents a promising avenue for research in cardiovascular health, with the potential to inform novel therapeutic strategies aimed at improving outcomes in patients with HTN and HF. Further research is necessary to elucidate the details of omentin-1 function and evaluate its potential in the treatment of cardiovascular disease. © The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature 2025.
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