{'fraction_non_alphanumeric': 0.03749098774333093, 'fraction_numerical': 0.01946647440519106, 'mean_word_length': 5.974874371859296, '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}}
Nitric oxide and vascular hypertrophy.

Cardiovascular diseases are the leading cause of morbidity and mortality in industrialized countries. Diseases of the heart, including coronary artery disease and myocardial infarction, rank number one, and cerebrovascular diseases number three, in the list of the 10 leading causes of death in the USA. Many of these cardiovascular endpoints are directly related to vascular alterations associated with atherosclerosis [1–3]. Thus, a profound understanding of the mechanisms leading to atherosclerosis is necessary to design strategies to prevent and treat atherosclerosis. Besides an inflammatory reaction within the wall of the affected arteries [4–6], proliferation and accumulation of vascular smooth muscle cells (VSMC) play an important role in the progression of lesion formation and the development of atherosclerosis [7,8]. Furthermore, neointima formation occurs in all arteries as a response to a wide variety of injuries [9], and ultimately leads to endothelial dysfunction. Pathogenic factors that facilitate endothelial dysfunction include atherosclerosis [10], hypertension [11–14], diabetes [15], inflammation [16,17], oxidative stress [18] and ageing [19]. Functionally, endothelial dysfunction is characterized by an impaired ability of the endothelium to synthesize and release vasoactive substances, such as nitric oxide [20].