How is Tempostatin relevant to heart disease?
Abnormal tissue repair in the heart can happen in two different clinical situations. In the first situation, re-narrowing (restenosis) of blood vessels may follow treatment for blockage of the vessel. In at least 25% of the 600,000 patients that undergo coronary artery angioplasty in the United States each year, the treated vessels re-narrow within a few months of the procedure. This restenosis results from the migration and proliferation of smooth muscle cells (stromal cells) that produce excessive and undesirable amounts of collagen. Tempostatin arrests the activation of the arterial smooth muscle cells, suppressing their migration, proliferation, and undesirable collagen type I production. In the second situation, chronic volume overload of the heart may trigger a replacement of the normal extra-cellular matrix with a thickened scar-like collagen mass. This response to volume and pressure overload eventually replaces the normal tissue structure and severely limits the ability of the
