{'fraction_non_alphanumeric': 0.04220499569336779, 'fraction_numerical': 0.01636520241171404, 'mean_word_length': 5.8352941176470585, '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}}
ACE2 as therapy for pulmonary arterial hypertension: the good outweighs the bad

Since its initial discovery 120 years ago, the understanding of the renin−angiotensin system (RAS) has advanced considerably. In recent years, the identification of new enzymes, peptides and receptors that are constituents of novel identified counterbalancing RAS pathways acting beyond the classical ACE (angiotensin-converting enzyme)/angiotensin (Ang)II/AT1 receptor axis have heralded a new era highlighting its importance in health and disease (figure 1). As a result, it is now well established that inhibition of the classical RAS and activation of the counterbalancing axes (alternative RAS), namely the ACE2−Ang-(1–7)−Mas receptor cascade and the AT2 signalling pathway are two feasible strategies demonstrating efficacies in various cardiovascular and pulmonary disease models, including in various preclinical models of pulmonary hypertension (PH) [1–6]. Based on this highly encouraging clinical proof-of-concept, there is now a clear plan to explore interventions that stimulate the ACE2–Ang-(1–7)–Mas pathway further in large clinical trials http://ow.ly/adXT30k1Z5h