Cardiac hypertrophy (CH) is an adaptive cardiac response to overload whose decompensation eventually leads to heart failure or sudden death. Recently, accumulating studies have indicated the implication of long noncoding RNAs (lncRNAs) in CH progression. MAGI1-IT1 is a newly-identified lncRNA that is highly associated with CH, while its specific role in CH progression remains masked. In this study, we uncovered that MAGI1-IT1 was distinctly downregulated in angiotensin (Ang) Ⅱ-induced hypertrophic H9c2 cells. Also, MAGI1-IT1 overexpression in Ang Ⅱtreated H9c2 cells strikingly abolished the enlarged surface area and the enhanced levels of hypertrophic markers such as ANP, BNP, and β-MHC. Mechanically, we found MAGI1-IT1 sponged miR-302e which was identified as a hypertrophyfacilitator here, and that miR-302e upregulation countervailed the inhibition of MAGI1-IT1 overexpression on hypertrophic cells. Moreover, it was confirmed that MAGI1-IT1 boosted DKK1 expression by absorbing miR-302e. Subsequently, we also illustrated that MAGI1-IT1 inactivated Wnt/beta-catenin signaling through a DKK1dependent pathway. Finally, both the DKK1 inhibition and LiCI (Wnt activator) supplement abrogated the hypertrophy-suppressive impact of MAGI1-IT1 on Ang Ⅱsimulated hypertrophic H9c2 cells. Jointly, our findings disclosed that MAGI1-IT1 functioned as a negative regulator in CH through inactivating Wnt/beta-catenin pathway via targeting miR-302e/DKK1 axis, revealing a novel road for CH treatment. K E Y W O R D S cardiac hypertrophy, DKK1, MAGI1-IT1, miR-302e, Wnt signaling

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Understanding urea decomposition is critical to achieve highly efficient selective catalytic reduction (SCR). The urea decomposition process in an exhaust pipe and in Cu‐zeolite and vanadia‐SCR (V‐SCR) was studied in engine test cells. The unconverted urea at the SCR inlet can be substantial at lower temperatures. HNCO and NH3 are two dominant products at the SCR inlet. Urea and HNCO continue to decompose in SCR catalysts, with a rate much faster than in the homogeneous stream. The HNCO hydrolysis process is extremely efficient in Cu‐zeolite SCR and the abundant NH3 from urea overdosing can improve the NOx conversion efficiency. While for V‐SCR, the HNCO hydrolysis reaction can become the rate‐limiting step (especially after aging), abundant urea at low temperatures impairs NOx reduction.

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