Arterial remodelling and inflammation in peripheral arterial disease

Rasheeda Mohd Zamin

    Research output: ThesisDoctoral Thesis

    528 Downloads (Pure)

    Abstract

    [Truncated abstract] Peripheral arterial disease (PAD) can lead to impaired perfusion to the lower limbs and remains an important cause for non-traumatic lower limb amputations. PAD is becoming known as an inflammatory disease with established biomarkers such as Creactive protein and osteoprotegerin (OPG). PAD is commonly associated with diabetes mellitus, which is thought to be a product of low-grade but chronic inflammation. Common pathological causes of PAD, which include atherosclerosis, are now linked to the presence of several inflammatory factors such as fractalkine receptor (CX3CR1) and monocyte chemotactic protein-1 receptor (now known as CCR2).
    Another common characteristic of PAD is arterial calcification, which previously received less attention but is now being investigated for the receptor activator of nuclear factor kappa-B (RANK), RANK ligand and OPG involvement as part of an active cellular regulation of the calcification process. Not only does atherosclerosis have a close association with inflammatory and immune-based regulation, but also there is strong evidence to suggest that arterial calcification is regulated by inflammatory factors. It is important to identify the specific inflammatory factors, which may play a role in the development and progression of PAD.

    Original languageEnglish
    QualificationDoctor of Philosophy
    Publication statusUnpublished - 2013

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