{'fraction_non_alphanumeric': 0.02328646748681898, 'fraction_numerical': 0.014499121265377855, 'mean_word_length': 5.984662576687117, '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}}
The Effect of Metformin on Cardiac Fibrosis via Differentiation of Cardiac Fibroblasts

It has been proved that metformin, commonly used in daily practice as an antidiabetic oral drug with antioxidant properties, has cardioprotective effects in patients with diabetic disease. A recent study investigated the effects of metformin on the expression of the receptor for advanced glycation end products (RAGE) and high mobility group box 1 protein (HMGB1) in hyperglycemia-treated neonatal rat ventricular myocytes [4] . Metformin significantly inhibited the increase of malondialdehyde, tumor necrosis factor-α, lactate dehydrogenase and creatine kinase levels induced by high glucose while inhibiting the decrease of superoxide dismutase level. The study concluded that metformin reduces hyperglycemia-induced cardiocyte injury by inhibiting the expression of RAGE and HMGB1 [4] . It is known that metformin, an antidiabetic agent, exhibits many cardioprotective properties. The least-known of these is the effect on cardiac fibroblast differentiation. Angiotensin II-induced differentiation of cardiac fibroblasts into myofibroblasts [5] We read the article ‘Protective effect of metformin on myocardial injury in metabolic syndrome patients following percutaneous coronary intervention’ by Li et al. [1] with interest. They investigated the hypothesis that pretreatment with metformin decreases postprocedural myocardial injury and improves clinical outcomes in metabolic syndrome patients following percutaneous coronary intervention. They demonstrated that a 7-day metformin pretreatment regimen (250 mg given 3 times a day) does indeed significantly reduce postprocedural myocardial injury and improves 1-year clinical outcomes in these patients. Many studies have shown that treatment with metformin improves cardiovascular outcomes and limits atherosclerosis in overweight patients with metabolic syndromes or diabetes. This observation has depended on the hypothesis that metformin has direct cardiovascular protective properties over and beyond a glucose-lowering effect. In addition, it consistently limits myocardial infarct size and reduces postinfarction remodeling [2, 3] . Received: October 13, 2014 Accepted: October 15, 2014 Published online: December 13, 2014