{'fraction_non_alphanumeric': 0.021213406873143825, 'fraction_numerical': 0.024183283835383963, 'mean_word_length': 5.698863636363637, '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}}
Letter by Wang et al Regarding Article, "A Novel Role of Cyclic Nucleotide Phosphodiesterase 10A in Pathological Cardiac Remodeling and Dysfunction".

Circulation. 2020;142:e34–e35. DOI: 10.1161/CIRCULATIONAHA.120.046614 e34 *Drs Wang and Yang contributed equally. Daxin Wang, MD* Xinquan Yang, MD* Xingyu Yu, MD To the Editor: We read the article by Chen et al1 with interest. The authors decipher a novel role of cyclic nucleotide phosphodiesterase 10A (PDE10A) in pathologic cardiac remodeling and highlight the potential therapeutic value of the selective inhibitor of PDE10A in the treatment of heart failure. Chronic pharmacologic inhibition of PDE10A could potentiate thermogenesis and improve insulin sensitivity, probably through stimulation of thermogenic gene expression in the brown adipocytes and promotion of browning of white adipocytes.2 Attenuating inflammation and improving insulin resistance in adipose tissue ameliorated cardiac dysfunction in a murine model of chronic heart failure.3 Thus we considered that further study aiming at evaluating the changes in metabolic state and energy homeostasis might provide a novel link between the heart and other organs, such as the hypothalamus–heart–adipose tissue axis, based on the findings presented by Chen et al,1 because weight loss has been regarded as a predictor of unfavorable outcomes in patients with heart failure with reduced ejection fraction.4 In light of the significant impact of PDE10A inhibitor on reduction of body weight,2 real-time monitoring of changes in body weight and evaluation of long-term survival rates are necessary, especially in patients with preexisting cardiac defects treated with pharmacologic PDE10A inhibitor (TP-10), for identifying the safety and application conditions of this drug. PDE10A has been identified as a candidate gene contributing to strong sex-specific differences in thyroid function and related pathologies.5 Thus investigating potential effects of PDE10A inhibition on the hypothalamic–pituitary–thyroid axis or sexual dimorphism in heart failure deserves more attention. We congratulate the authors for discovering a novel therapeutic strategy for antagonizing the progression of pathologic cardiac remodeling and hope that our ideas will stimulate findings in further experimental research on the clinical use of PDE10A inhibition.