{'fraction_non_alphanumeric': 0.02865612648221344, 'fraction_numerical': 0.00691699604743083, 'mean_word_length': 5.9862068965517246, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Gene Therapy for All Aspects of Vein‐Graft Disease

Abstract  Gene therapy could improve human saphenous vein (HSV) coronary vein‐graft patency by reducing early thrombosis, neointimal hyperplasia and atherosclerosis. Mouse and rabbit models use veins with much thinner walls than pig or HSVs but atherosclerosis can be more easily induced; none of these models shows early thrombosis. Prostacyclin synthase, tissue factor pathway inhibitor, and tissue plasminogen activator might decrease thrombus formation. Tissue inhibitors of metalloproteinases (TIMPs) reduce intimal migration of smooth muscle cells, while TIMP‐3 and the p53 tumor suppressor protein promote apoptosis. Prostacyclin synthase and nitric oxide synthase, and cell cycle inhibitors, such as E2F decoy oligonucleotides (D‐E2F), reduce neointima formation. This might be enough by itself to decrease later atherosclerosis. Alternatively, direct targeting with nitric oxide synthase, decoy adhesion molecules, or interleukin‐10 might be possible.