» Articles » PMID: 38114042

Adipsin in the Pathogenesis of Cardiovascular Diseases

Overview
Authors
Affiliations
Soon will be listed here.
Abstract

Adipsin is an adipokine predominantly synthesized in adipose tissues and released into circulation. It is also known as complement factor-D (CFD), acting as the rate-limiting factor in the alternative complement pathway and exerting essential functions on the activation of complement system. The deficiency of CFD in humans is a very rare condition. However, complement overactivation has been implicated in the etiology of numerous disorders, including cardiovascular disease (CVD). Increased circulating level of adipsin has been reported to promote vascular derangements, systemic inflammation, and endothelial dysfunction. Prospective and case-control studies showed that this adipokine is directly associated with all-cause death and rehospitalization in patients with coronary artery disease. Adipsin has also been implicated in pulmonary arterial hypertension, abdominal aortic aneurysm, pre-eclampsia, and type-2 diabetes which is a major risk factor for CVD. Importantly, serum adipsin has been recognized as a unique prognostic marker for assessing cardiovascular diseases. At present, there is paucity of experimental evidence about the precise role of adipsin in the etiology of CVD. However, this mini review provides some insight on the contribution of adipsin in the pathogenesis of CVD and highlights its role on endothelial, smooth muscle and immune cells that mediate cardiovascular functions.

Citing Articles

Murine Model Insights: Identifying Dusp15 as a Novel Biomarker for Diabetic Cardiomyopathy Uncovered Through Integrated Omics Analysis and Experimental Validation.

Zhu L, Dong Y, Guo H, Qiu J, Guo J, Hu Y Diabetes Metab Syndr Obes. 2025; 18:515-527.

PMID: 39990179 PMC: 11847420. DOI: 10.2147/DMSO.S501563.


Exploring How Adipose Tissue, Obesity, and Gender Influence the Immune Response to Vaccines: A Comprehensive Narrative Review.

De Sanctis J, Balda Noria G, Garcia A Int J Mol Sci. 2025; 26(2).

PMID: 39859575 PMC: 11765591. DOI: 10.3390/ijms26020862.


Environmental Enrichment Normalizes Metabolic Function in the Murine Model of Prader-Willi Syndrome Magel2-Null Mice.

Queen N, Zou X, Huang W, Mohammed T, Cao L Endocrinology. 2025; 166(3).

PMID: 39801003 PMC: 11808065. DOI: 10.1210/endocr/bqaf001.


Multifaced roles of adipokines in endothelial cell function.

Yan Y, Wang L, Zhong N, Wen D, Liu L Front Endocrinol (Lausanne). 2024; 15:1490143.

PMID: 39558976 PMC: 11570283. DOI: 10.3389/fendo.2024.1490143.

References
1.
Kwan W, van der Touw W, Heeger P . Complement regulation of T cell immunity. Immunol Res. 2012; 54(1-3):247-53. PMC: 4081859. DOI: 10.1007/s12026-012-8327-1. View

2.
Feridooni T, Zamzam A, Popkov M, Syed M, Djahanpour N, Wheatcroft M . Plasma complement component C2: a potential biomarker for predicting abdominal aortic aneurysm related complications. Sci Rep. 2022; 12(1):21252. PMC: 9732295. DOI: 10.1038/s41598-022-24698-1. View

3.
Hertle E, Arts I, van der Kallen C, Feskens E, Schalkwijk C, Stehouwer C . The alternative complement pathway is longitudinally associated with adverse cardiovascular outcomes. The CODAM study. Thromb Haemost. 2015; 115(2):446-57. DOI: 10.1160/TH15-05-0439. View

4.
Lin Z, Fukuda N, Jin X, Yao E, Ueno T, Endo M . Complement 3 is involved in the synthetic phenotype and exaggerated growth of vascular smooth muscle cells from spontaneously hypertensive rats. Hypertension. 2004; 44(1):42-7. DOI: 10.1161/01.HYP.0000129540.83284.ca. View

5.
Korman B, Marangoni R, Hinchcliff M, Shah S, Carns M, Hoffmann A . Brief Report: Association of Elevated Adipsin Levels With Pulmonary Arterial Hypertension in Systemic Sclerosis. Arthritis Rheumatol. 2017; 69(10):2062-2068. PMC: 5748338. DOI: 10.1002/art.40193. View