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MIAT, a potent CVD-promoting lncRNA

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Abstract

The initial identification of long non-coding RNA myocardial infarction associated transcript (MIAT) as a genetic risk factor of myocardial infarction has made this lncRNA (designated as lncR-MIAT here) a focus of intensive studies worldwide. Emerging evidence supports that lncR-MIAT is susceptible in its expression to multiple deleterious factors like angiotensin II, isoproterenol, hypoxia, and infection and is anomaly overexpressed in serum, plasma, blood cells and myocardial tissues under a variety of cardiovascular conditions including myocardial infarction, cardiac hypertrophy, diabetic cardiomyopathy, dilated cardiomyopathy, sepsis cardiomyopathy, atrial fibrillation and microvascular dysfunction. Experimental results consistently demonstrated that upregulation of lncR-MIAT plays active roles in the pathological processes of the cardiovascular system and knockdown of this lncRNA effectively ameliorates the adverse conditions. The available data revealed that lncR-MIAT acts through multiple mechanisms such as competitive endogenous RNA, natural antisense RNA and RNA/protein interactions. Moreover, the functional domains of lncR-MIAT accounting for certain specific cellular functions of the full-length transcript have been identified and characterized. These insights will not only tremendously advance our understanding of lncRNA biology and pathophysiology, but also offer good opportunities for more innovative and precise design of agents that have the potential to be developed into new drugs for better therapy of cardiovascular diseases (CVDs) in the future. Herein, we provide an overview of lncR-MIAT, focusing on its roles in cardiovascular diseases, underline the unique cellular/molecular mechanisms for its actions, and speculate the perspectives about the translational studies on the potential diagnostic and therapeutic applications of lncR-MIAT.

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The data sets used and/or analyzed during the current study are available from the corresponding author on reasonable request.

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Acknowledgements

The authors greatly thank Prof. Zhiguo Wang for continued support and valuable advice of this manuscript.

Funding

This work was supported by the Funds for National Key Research and Development Program of China (2017YFC1307403 to Baofeng Yang, 2017YFC1702003 to Yong Zhang); the Key Program of National Natural Science Foundation of China (81730012 to Yong Zhang); the National Natural Science Foundation of China (81861128022, 81570301, 81570399 to Yong Zhang); and Qiqihar Academy of Medical Sciences Project (QMSI2020B-04 to Chao Yang).

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Authors and Affiliations

  1. Department of Pharmacology (The State-Province Key Laboratories of Biomedicine Pharmaceutics of China, Key Laboratory of Cardiovascular Research, Ministry of Education), College of Pharmacy, Harbin Medical University, 157 Baojian Road, Nangang District, Harbin, Heilongjiang, 150081, People’s Republic of China

    Chao Yang, Yong Zhang & Baofeng Yang

  2. Department of Biochemistry, Qiqihar Medical University, Qiqihar, 161000, Heilongjiang, People’s Republic of China

    Chao Yang

  3. Institute of Metabolic Disease, Heilongjiang Academy of Medical Science, Harbin, 150086, People’s Republic of China

    Yong Zhang

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  1. Chao Yang
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  2. Yong Zhang
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  3. Baofeng Yang
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BY conceived idea of the article. CY performed the literature search and wrote the manuscript. YZ critically revised the work. All authors approved the final version of the paper.

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Correspondence to Baofeng Yang.

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Yang, C., Zhang, Y. & Yang, B. MIAT, a potent CVD-promoting lncRNA. Cell. Mol. Life Sci. 79, 43 (2022). https://doi.org/10.1007/s00018-021-04046-8

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