期刊
JOURNAL OF CARDIOVASCULAR PHARMACOLOGY
卷 56, 期 6, 页码 589-595出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/FJC.0b013e3181f8d173
关键词
microRNA; heart development; reactive hypertrophy; biomarker
资金
- NHLBI NIH HHS [R01 HL080008, R01 HL059888-06, R01 HL087871-05, R01 HL059888-12, R01 HL087871-01, R01 HL080008-03, R01 HL080008-04, R01 HL059888-10, R01 HL059888-05, RC2 HL102222-02, R01 HL059888, R01 HL059888-11, R01 HL059888-07, R01 HL087871, R01 HL059888-02, R01 HL059888-09A1W1, R01 HL087871-06, R01 HL059888-09A1, R01 HL080008-02, R01 HL059888-01A1, RC2 HL102222, R01 HL080008-01A1, R01 HL087871-04, R01 HL087871-02, R01 HL080008-05, R01 HL059888-03, R01 HL059888-08, RC2 HL102222-01, R01 HL087871-03, R01 HL059888-04, R01 HL080008-06] Funding Source: Medline
MicroRNAs (miRs) regulate protein expression by inhibiting translation of expressed mRNAs. Targeting by one or more miRs of multiple mRNA transcripts encoding proteins with common functions confers nodal control over cardiac development and stress response. Dynamic coregulation of miRs and their mRNA targets has complicated understanding their biology but also provides opportunities for clinical diagnostics and therapeutics. Here, the biology of miRs is reviewed as it relates to the cardiac system, recent findings are described that illuminate miR control of cardiac development and myofiber identity, and the clinical ramifications of miR expression profiling are illustrated.
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