microRNA在心脏重塑中的研究进展
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摘要
microRNAs(miRNAs)通过对其靶基因的转录后调控参与胚胎发育、细胞增殖、分化及凋亡等过程,与心血管疾病的发生发展密切相关。心脏重塑目前缺乏有效的治疗靶点和有效的诊疗标志物,并且心脏重塑的机制研究还不够深入。目前发现miRNAs可通过不同的分子机制调节心肌纤维化、心肌肥大以及能量代谢调节重塑。
microRNAs(miRNAs) are involved in embryonic development, cell proliferation, differentiation and apoptosis through post-transcriptional regulation of their target genes, and are closely related to the occurrence and development of cardiovascular diseases. Cardiac remodeling currently lacks effective therapeutic targets and effective diagnostic markers, and the mechanism of cardiac remodeling is not well understand. It has been found that miRNAs can regulate myocardial fibrosis, cardiac hypertrophy, and energy metabolism and remodeling through different molecular mechanisms.
microRNAs(miRNAs) are involved in embryonic development, cell proliferation, differentiation and apoptosis through post-transcriptional regulation of their target genes, and are closely related to the occurrence and development of cardiovascular diseases. Cardiac remodeling currently lacks effective therapeutic targets and effective diagnostic markers, and the mechanism of cardiac remodeling is not well understand. It has been found that miRNAs can regulate myocardial fibrosis, cardiac hypertrophy, and energy metabolism and remodeling through different molecular mechanisms.
引文
[1] Saxena A, Tabin CJ. miRNA-processing enzyme Dicer is necessary for cardiac outflow tract alignment and chamber septation[J]. Proc Natl Acad Sci U S A, 2010, 107:87-91.
[2] Zhang Y, Huang XR, Wei LH, et al. miR-29b as a therapeutic agent for angiotensin II-induced cardiac fbrosis by targeting TGF-beta/Smad3 signaling[J]. Mol Ther, 2014, 22:974-985.
[3] Yuan J, Chen H, Ge D, et al. miR-21 promotes cardiac fibrosis after myocardial infarction via targeting smad7[J]. Cell Physiol Biochem, 2017, 42:2207-2219.
[4] Garcia R, Nistal JF, Merino D, et al. p-SMAD2/3 and DICER promote pre-miR-21 processing during pressure overload-associated myocardial remodeling[J]. Biochim Biophys Acta, 2015, 1852:1520-1530.
[5] Lorenzen JM, Schauerte C, Hubner A, et al. Osteopontin is indispensible for AP1-mediated angiotensin II-related miR-21 transcription during cardiac fbrosis[J]. Eur Heart J, 2015, 36:2184-2196.
[6] Cao W, Shi P, Ge JJ. miR-21 enhances cardiac fibrotic remodeling and fibroblast proliferation via CADM1/STAT3 pathway[J]. BMC Cardiovasc Aisord, 2017, 17:88-99.
[7] Verma SK, Garikipati VNS, Krishnamurthy P, et al. Interleukin 10 inhibits bone marrow fibroblast progenitor cell-mediated cardiac fibrosis in pressure overloaded myocardium[J]. Circulation, 2017, 136:940-953.
[8] Chen Z, Lu S, Xu M, et al. Role of miR-24, furin, and transforming growth factor-beta1 signal pathway in fibrosis after cardiac infarction[J]. Med Sci Monit, 2017, 23:65-70.
[9] Feng B, Chen S, Gordon AD, et al. miR-146a mediates inflammatory changes and fibrosis in the heart in diabetes[J]. J Mol Cell Cardiol, 2017, 105:70-76.
[10] Li L, Bounds KR, Chatterjee P, et al. MicroRNA-130a, a potential antifibrotic target in cardiac fibrosis[J]. J Am Heart Assoc, 2017, 6:6763-6778.
[11] Nishiga M, Horie T, Kuwabara Y, et al. MicroRNA-33 controls adaptive fibrotic response in the remodeling heart by preserving lipid raft cholesterol[J]. Circ Res, 2017, 120:835-847.
[12] Verjans R, Peters T, Beaumont FJ, et al. MicroRNA-221/222 family counteracts myocardial fibrosis in pressure overload-induced heart failure[J]. Hypertension, 2018, 71:280-288.
[13] Lai KB, Sanderson JE, Izzat MB, et al. Micro-RNA and mRNA myocardial tissue expression in biopsy specimen from patients with heart failure[J]. Int J Cardiol, 2015, 199:79-83.
[14] Zaglia T, Ceriotti P, Campo A, et al. Content of mitochondrial calcium uniporter (MCU) in cardiomyocytes is regulated by microRNA-1 in physiologic and pathologic hypertrophy[J]. Proc Natl Acad Sci U S A, 2017,114:e9006-e9015.
[15] Derda AA, Thum S, Lorenzen JM, et al. Blood-based microRNA signatures differentiate various forms of cardiac hypertrophy[J]. Int J Cardiol, 2015, 196:115-122.
[16] Liu Y, Liang Y, Zhang JF, et al. MicroRNA-133 mediates cardiac diseases: mechanisms and clinical implications[J]. Exp Cell Res, 2017, 354:65-70.
[17] Li N, Zhou H, Tang Q. miR-133: a suppressor of cardiac remodeling?[J]. Fron in Pharmacol, 2018, 9:903-922.
[18] Van Middendorp LB, Kuiper M, Munts C, et al. Local microRNA-133a downregulation is associated with hypertrophy in the dyssynchronous heart[J]. ESC Heart Failure, 2017, 4:241-251.
[19] Bao Q, Zhao M, Chen L, et al. MicroRNA-297 promotes cardiomyocyte hypertrophy via targeting sigma-1 receptor[J]. Life Sci, 2017, 175:1-10.
[20] Heggermont WA, Papageorgiou AP, Quaegebeur A, et al. Inhibition of microRNA-146a and overexpression of its target dihydrolipoyl succinyltransferase protect against pressure overload-induced cardiac hypertrophy and dysfunction[J]. Circulation, 2017, 136:747-761.
[21] Li AL, Lv JB, Gao L. miR-181a mediates AngII-induced myocardial hypertrophy by mediating autophagy[J]. Eur Rev Med Pharmacol Sci, 2017, 21:5462-5470.
[22] Wang D, Zhai G, Ji Y, et al. microRNA-10a targets t-box 5 to inhibit the development of cardiac hypertrophy[J]. Int Heart J, 2017, 58:100-106.
[23] Das S, Kohr M, Dunkerly-Eyring B, et al. Divergent effects of miR-181 family members on myocardial function through protective cytosolic and detrimental mitochondrial microRNA targets[J]. J Am Heart Assoc, 2017, 6:4694-4711.
[24] Azzouzi H, Leptidis S, Dirkx E, et al. The hypoxia-inducible microRNA cluster miR-199a-214 targets myo-cardial PPARδ and impairs mitochondrial fatty acid oxidation[J]. Cell Metab, 2013, 18:341-354.
[25] Demkes CJ, Van RE. MicroRNA-146a as a regulator of cardiac energy metabolism[J]. Circulation, 2017, 136:762-764.
[2] Zhang Y, Huang XR, Wei LH, et al. miR-29b as a therapeutic agent for angiotensin II-induced cardiac fbrosis by targeting TGF-beta/Smad3 signaling[J]. Mol Ther, 2014, 22:974-985.
[3] Yuan J, Chen H, Ge D, et al. miR-21 promotes cardiac fibrosis after myocardial infarction via targeting smad7[J]. Cell Physiol Biochem, 2017, 42:2207-2219.
[4] Garcia R, Nistal JF, Merino D, et al. p-SMAD2/3 and DICER promote pre-miR-21 processing during pressure overload-associated myocardial remodeling[J]. Biochim Biophys Acta, 2015, 1852:1520-1530.
[5] Lorenzen JM, Schauerte C, Hubner A, et al. Osteopontin is indispensible for AP1-mediated angiotensin II-related miR-21 transcription during cardiac fbrosis[J]. Eur Heart J, 2015, 36:2184-2196.
[6] Cao W, Shi P, Ge JJ. miR-21 enhances cardiac fibrotic remodeling and fibroblast proliferation via CADM1/STAT3 pathway[J]. BMC Cardiovasc Aisord, 2017, 17:88-99.
[7] Verma SK, Garikipati VNS, Krishnamurthy P, et al. Interleukin 10 inhibits bone marrow fibroblast progenitor cell-mediated cardiac fibrosis in pressure overloaded myocardium[J]. Circulation, 2017, 136:940-953.
[8] Chen Z, Lu S, Xu M, et al. Role of miR-24, furin, and transforming growth factor-beta1 signal pathway in fibrosis after cardiac infarction[J]. Med Sci Monit, 2017, 23:65-70.
[9] Feng B, Chen S, Gordon AD, et al. miR-146a mediates inflammatory changes and fibrosis in the heart in diabetes[J]. J Mol Cell Cardiol, 2017, 105:70-76.
[10] Li L, Bounds KR, Chatterjee P, et al. MicroRNA-130a, a potential antifibrotic target in cardiac fibrosis[J]. J Am Heart Assoc, 2017, 6:6763-6778.
[11] Nishiga M, Horie T, Kuwabara Y, et al. MicroRNA-33 controls adaptive fibrotic response in the remodeling heart by preserving lipid raft cholesterol[J]. Circ Res, 2017, 120:835-847.
[12] Verjans R, Peters T, Beaumont FJ, et al. MicroRNA-221/222 family counteracts myocardial fibrosis in pressure overload-induced heart failure[J]. Hypertension, 2018, 71:280-288.
[13] Lai KB, Sanderson JE, Izzat MB, et al. Micro-RNA and mRNA myocardial tissue expression in biopsy specimen from patients with heart failure[J]. Int J Cardiol, 2015, 199:79-83.
[14] Zaglia T, Ceriotti P, Campo A, et al. Content of mitochondrial calcium uniporter (MCU) in cardiomyocytes is regulated by microRNA-1 in physiologic and pathologic hypertrophy[J]. Proc Natl Acad Sci U S A, 2017,114:e9006-e9015.
[15] Derda AA, Thum S, Lorenzen JM, et al. Blood-based microRNA signatures differentiate various forms of cardiac hypertrophy[J]. Int J Cardiol, 2015, 196:115-122.
[16] Liu Y, Liang Y, Zhang JF, et al. MicroRNA-133 mediates cardiac diseases: mechanisms and clinical implications[J]. Exp Cell Res, 2017, 354:65-70.
[17] Li N, Zhou H, Tang Q. miR-133: a suppressor of cardiac remodeling?[J]. Fron in Pharmacol, 2018, 9:903-922.
[18] Van Middendorp LB, Kuiper M, Munts C, et al. Local microRNA-133a downregulation is associated with hypertrophy in the dyssynchronous heart[J]. ESC Heart Failure, 2017, 4:241-251.
[19] Bao Q, Zhao M, Chen L, et al. MicroRNA-297 promotes cardiomyocyte hypertrophy via targeting sigma-1 receptor[J]. Life Sci, 2017, 175:1-10.
[20] Heggermont WA, Papageorgiou AP, Quaegebeur A, et al. Inhibition of microRNA-146a and overexpression of its target dihydrolipoyl succinyltransferase protect against pressure overload-induced cardiac hypertrophy and dysfunction[J]. Circulation, 2017, 136:747-761.
[21] Li AL, Lv JB, Gao L. miR-181a mediates AngII-induced myocardial hypertrophy by mediating autophagy[J]. Eur Rev Med Pharmacol Sci, 2017, 21:5462-5470.
[22] Wang D, Zhai G, Ji Y, et al. microRNA-10a targets t-box 5 to inhibit the development of cardiac hypertrophy[J]. Int Heart J, 2017, 58:100-106.
[23] Das S, Kohr M, Dunkerly-Eyring B, et al. Divergent effects of miR-181 family members on myocardial function through protective cytosolic and detrimental mitochondrial microRNA targets[J]. J Am Heart Assoc, 2017, 6:4694-4711.
[24] Azzouzi H, Leptidis S, Dirkx E, et al. The hypoxia-inducible microRNA cluster miR-199a-214 targets myo-cardial PPARδ and impairs mitochondrial fatty acid oxidation[J]. Cell Metab, 2013, 18:341-354.
[25] Demkes CJ, Van RE. MicroRNA-146a as a regulator of cardiac energy metabolism[J]. Circulation, 2017, 136:762-764.