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Heparanase: A Novel Therapeutic Target for the Treatment of Atherosclerosis

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posted on 2023-06-28, 02:39 authored by Tien NguyenTien Nguyen, S Paone, E Chan, Ivan PoonIvan Poon, Amy BaxterAmy Baxter, SR Thomas, Mark HulettMark Hulett
Cardiovascular disease (CVD) is the leading cause of death and disability worldwide, and its management places a huge burden on healthcare systems through hospitalisation and treatment. Atherosclerosis is a chronic inflammatory disease of the arterial wall resulting in the formation of lipid-rich, fibrotic plaques under the subendothelium and is a key contributor to the development of CVD. As such, a detailed understanding of the mechanisms involved in the development of atherosclerosis is urgently required for more effective disease treatment and prevention strategies. Heparanase is the only mammalian enzyme known to cleave heparan sulfate of heparan sulfate proteoglycans, which is a key component of the extracellular matrix and basement membrane. By cleaving heparan sulfate, heparanase contributes to the regulation of numerous physiological and pathological processes such as wound healing, inflammation, tumour angiogenesis, and cell migration. Recent evidence suggests a multifactorial role for heparanase in atherosclerosis by promoting underlying inflammatory processes giving rise to plaque formation, as well as regulating lesion stability. This review provides an up-to-date overview of the role of heparanase in physiological and pathological processes with a focus on the emerging role of the enzyme in atherosclerosis.

Funding

This work was supported by the Medical Research Future Fund Cardiovascular Health Mission Grant (MRF2008787).

History

Publication Date

2022-10-01

Journal

Cells

Volume

11

Issue

20

Article Number

3198

Pagination

22p.

Publisher

MDPI

ISSN

2073-4409

Rights Statement

© 2022 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).

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