Project Details
Description
Calcification is a common occurrence in end-stage renal failure and shows a strong correlation with declining renal function.
It often results in a diverse range of pathologies including calcific uraemic arteriolopathy, solid as well as extra-osseous soft tissue calcification of which vascular calcification (VC) is the most common and often the most clinically relevant corollary.
The existence of VC in chronic kidney disease (CKD) results in increased arterial stiffness, becoming predictive of secondary cardio-vascular complications with high morbidity and mortality.
The precise mechanisms that lead to VC in CKD subjects are poorly understood but it is accepted to be a delicate and well-controlled biological process that results in smooth muscle cells (SMCs) gaining an osteoblastic phenotype.
These complex changes may be regulated in vivo by circulating factors in plasma but it is not entirely clear how the various molecules act, nor is the complex interplay amongst the key factors established. Moreover, it is not clear whether the presence of the various factors in serum may be sufficient to regulate calcification outside of disease settings.
Our research in this area is aimed at establishing the in vitro calcific potential (ie ability to induce calcification) of serum and determining whether in vitro calcific potential correlates with the degree of renal impairment in vivo.
In parallel, we are also interested in identifying critical biomarker surrogates and mechanisms responsible for the calcific potential of the serum. This may lead to the development of diagnostic tools and inform therapeutic strategies.
It often results in a diverse range of pathologies including calcific uraemic arteriolopathy, solid as well as extra-osseous soft tissue calcification of which vascular calcification (VC) is the most common and often the most clinically relevant corollary.
The existence of VC in chronic kidney disease (CKD) results in increased arterial stiffness, becoming predictive of secondary cardio-vascular complications with high morbidity and mortality.
The precise mechanisms that lead to VC in CKD subjects are poorly understood but it is accepted to be a delicate and well-controlled biological process that results in smooth muscle cells (SMCs) gaining an osteoblastic phenotype.
These complex changes may be regulated in vivo by circulating factors in plasma but it is not entirely clear how the various molecules act, nor is the complex interplay amongst the key factors established. Moreover, it is not clear whether the presence of the various factors in serum may be sufficient to regulate calcification outside of disease settings.
Our research in this area is aimed at establishing the in vitro calcific potential (ie ability to induce calcification) of serum and determining whether in vitro calcific potential correlates with the degree of renal impairment in vivo.
In parallel, we are also interested in identifying critical biomarker surrogates and mechanisms responsible for the calcific potential of the serum. This may lead to the development of diagnostic tools and inform therapeutic strategies.
| Status | Active |
|---|---|
| Effective start/end date | 1/01/13 → … |
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