Myxomatous degenerative mitral valve disease (MMVD) is a common heart disease in dogs. Although several morphological similarities occur between human and canine MMVD differences exist. However, in advanced stages the accu- mulation of proteoglycans is the main finding in both species.
The extracellular matrix (ECM) in normal canine and human mitral valves is similar. In MMVD of both species proteoglycans is the major alteration, although specific changes in collagen distribution exists.
The valvular expression pattern of matrix metalloproteinases (MMPs) and of their inhibitors (TIMPs) differs, in part, between dogs and humans. The MMPs and TIMPs expression patterns are similar in normal canine and human mitral valves, but they are quite different during degenerative progression.
Valve endothelial cells (VEC) and interstitial cells (VIC) are phenotypically trans- formed in canine and human MMVD. Inflammation is an unlikely cause of valve degeneration in humans and dogs. There are several lines of evidence suggesting that transforming growth factor b1 (TGF b1) and serotonin signaling may mediate valve degeneration in humans and dogs.
Although human and canine MMVD share structural similarities, there are some differences in ECM changes, enzyme expression and cell transformation, which may reflect a varied pathogenesis of these diseases.
During the course of both canine and human aging, the mitral valve remodels in generally predictable ways. The connection between these aging changes and the morbidity and mortality that accompany pathologic conditions has not been made clear. By exploring work that has investigated the specific valvular changes in both age and disease, with respect to the cells and the extra- cellular matrix found within the mitral valve, heretofore unexplored connections between age and myxomatous valve disease can be found. This review addresses several studies that have been conducted to explore such age and disease related changes in extracellular matrix, valvular endothelial and interstitial cells, and valve innervation, and also reviews attempts to correlate aging and myxomatous disease. Such connections can highlight avenues for future research and help provide insight as to when an individual diverts from an aging pattern into a diseased pathway. Recognizing these patterns and opportunities could result in earlier intervention and the hope of reduced morbidity and mortality for patients.
Patrick S. Connell, BS a, Richard I. Han, PhD b, K. Jane Grande-Allen, PhD
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