{'fraction_non_alphanumeric': 0.016039481801357187, 'fraction_numerical': 0.0006169031462060457, 'mean_word_length': 5.96137339055794, '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}}
lncRNA Chronos Exacerbates Pathological Cardiac Dysfunction and Fibrosis

Long non‐coding RNAs (lncRNAs) are a recently discovered class of genes involved in epigenetic modifications, the regulation of transcription and translation, as well as RNA metabolism. Importantly, the expression of many lncRNAs are known to be developmentally regulated with cell and tissue type specificity and to be dysregulated under pathological conditions. Our previous work identified Chronos as a muscle enriched and aging‐induced, Akt1‐inhibited lncRNA that negatively regulates myogenesis. Testing the hypothesis that Chronos expression is deleterious, we generated Chronos deficient mice and subjected them to transverse aortic constriction (TAC) in order to study the role of Chronos in cardiac hypertrophy and myocardial remodeling. Preliminary data indicate that at early timepoints, Chronos deficient mice have less interstitial fibrosis, as indicated by Masson's Trichrome staining and qPCR analysis of extracellular matrix genes, as compared to WT controls, while still exhibiting hypertrophic growth. Pilot studies at late timepoints indicate no statistical difference between WT and Chronos deficient mice with regard to cardiac hypertrophy or interstitial fibrosis. These data suggest that lncRNA Chronos may play a role in the promoting the initial phases of interstitial fibrosis in response to cellular stress, rather than replacement fibrosis following cardiomyocyte apoptosis. Future studies will examine the role of Chronos in both the early and late stages of myocardial remodeling and compensatory cardiac hypertrophy.