Key result
This review highlights the structural, biomechanical, and molecular signaling changes, such as serotonin and TGFβ pathways, involved in the progression of canine myxomatous mitral valve disease.
Why the study?
While extensive research has focused on echocardiography and medical therapy for myxomatous mitral valve disease in dogs, less known information on the mitral valve, surgical approaches, devices, and molecular mechanisms warranted synthesis.
This review provides a comprehensive overview of the anatomy, biomechanics, and molecular mechanisms underlying myxomatous mitral valve disease in dogs.
Extends molecular insights into canine MMVD; leaves open whether targeting serotonin or TGFβ pathways alters progression.
Myxomatous mitral valve disease (MMVD) is the most common heart alteration in dogs. A vast extent of research has been focused on echocardiographic tissue Doppler and strain indices and the medical treatment of this condition, which are beyond the scope of this article. This review intends to include less known information of the mitral valve, acknowledge the American College of Veterinary Internal Medicine (ACVIM) consensus on MMVD and state different surgical approaches and devices, all valuable information for small animal clinicians and cardiologists. Also, during the last decade studies have been oriented towards to understand valve’s mechanical structure and function, genes involved in the etiology and molecular signaling pathways. Advances have been made in understanding the mitral valve, but more assessment and efforts are needed in this specific area.
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P. et al. (2019) conducted a review in Myxomatous mitral valve disease (MMVD). This review highlights the structural, biomechanical, and molecular signaling changes, such as serotonin and TGFβ pathways, involved in the progression of canine myxomatous mitral valve disease.
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