MicroRNA and vascular remodelling in acute vascular injury and pulmonary vascular remodelling

RA McDonald, A Hata, MR MacLean… - Cardiovascular …, 2012 - academic.oup.com
RA McDonald, A Hata, MR MacLean, NW Morrell, AH Baker
Cardiovascular research, 2012academic.oup.com
Vascular remodelling is an integral pathological process central to a number of
cardiovascular diseases. The complex interplay between distinct cell populations in the
vessel wall following vascular injury leads to inflammation, cellular dysfunction, pro-growth
signals in the smooth muscle cell (SMC) compartment, and the acquisition of a synthetic
phenotype. Although the signals for vascular remodelling are diverse in different
pathological contexts, SMC proliferation and migration are consistently observed. It is …
Abstract
Vascular remodelling is an integral pathological process central to a number of cardiovascular diseases. The complex interplay between distinct cell populations in the vessel wall following vascular injury leads to inflammation, cellular dysfunction, pro-growth signals in the smooth muscle cell (SMC) compartment, and the acquisition of a synthetic phenotype. Although the signals for vascular remodelling are diverse in different pathological contexts, SMC proliferation and migration are consistently observed. It is therefore critical to elucidate key mechanisms central to these processes. MicroRNAs (miRNAs) are small non-coding sequences of RNA that have the capacity to regulate many genes, pathways, and complex biological networks within cells, acting either alone or in concert with one another. In diseases such as cancer and cardiac disease, the role of miRNA in disease pathogenesis has been documented in detail. In contrast, despite a great deal of interest in miRNA, relatively few studies have directly assessed the role of miRNA in vascular remodelling. The potential for modulation of miRNA to achieve therapeutic benefits in this setting is attractive. Here, we focus on the role of miRNA in vascular inflammation and remodelling associated with acute vascular injury (vein graft disease, angioplasty restenosis, and in-stent restenosis) as well as in vascular remodelling associated with the development of pulmonary arterial hypertension.
Oxford University Press